HCSGD entry for PTEN

1. General information

Official gene symbol	PTEN
Entrez ID	5728
Gene full name	phosphatase and tensin homolog
Other gene symbols	10q23del BZS CWS1 DEC GLM2 MHAM MMAC1 PTEN1 TEP1
Links to Entrez Gene	Links to Entrez Gene

2. Neighbors in the network

This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID	GO term	Evidence	Category
GO:0000079	Regulation of cyclin-dependent protein serine/threonine kinase activity	TAS	biological_process
GO:0000287	Magnesium ion binding	IEA	molecular_function
GO:0001525	Angiogenesis	IEA	biological_process
GO:0001933	Negative regulation of protein phosphorylation	IDA	biological_process
GO:0002902	Regulation of B cell apoptotic process	IEA	biological_process
GO:0004438	Phosphatidylinositol-3-phosphatase activity	IDA	molecular_function
GO:0004721	Phosphoprotein phosphatase activity	IDA	molecular_function
GO:0004722	Protein serine/threonine phosphatase activity	IDA	molecular_function
GO:0004725	Protein tyrosine phosphatase activity	IDA	molecular_function
GO:0005161	Platelet-derived growth factor receptor binding	IEA	molecular_function
GO:0005515	Protein binding	IPI	molecular_function
GO:0005634	Nucleus	IDA	cellular_component
GO:0005737	Cytoplasm	IDA TAS	cellular_component
GO:0005739	Mitochondrion	IEA	cellular_component
GO:0005829	Cytosol	TAS	cellular_component
GO:0005886	Plasma membrane	IDA	cellular_component
GO:0006470	Protein dephosphorylation	IDA TAS	biological_process
GO:0006644	Phospholipid metabolic process	TAS	biological_process
GO:0006661	Phosphatidylinositol biosynthetic process	TAS	biological_process
GO:0006915	Apoptotic process	ISS	biological_process
GO:0007092	Activation of mitotic anaphase-promoting complex activity	IDA	biological_process
GO:0007173	Epidermal growth factor receptor signaling pathway	TAS	biological_process
GO:0007270	Neuron-neuron synaptic transmission	ISS	biological_process
GO:0007416	Synapse assembly	ISS	biological_process
GO:0007417	Central nervous system development	ISS	biological_process
GO:0007507	Heart development	ISS	biological_process
GO:0007568	Aging	IEA	biological_process
GO:0007584	Response to nutrient	IEA	biological_process
GO:0007611	Learning or memory	ISS	biological_process
GO:0007613	Memory	IEA	biological_process
GO:0007626	Locomotory behavior	ISS	biological_process
GO:0008138	Protein tyrosine/serine/threonine phosphatase activity	IEA	molecular_function
GO:0008283	Cell proliferation	TAS	biological_process
GO:0008284	Positive regulation of cell proliferation	ISS	biological_process
GO:0008285	Negative regulation of cell proliferation	IDA IMP	biological_process
GO:0008289	Lipid binding	IEA	molecular_function
GO:0008543	Fibroblast growth factor receptor signaling pathway	TAS	biological_process
GO:0009749	Response to glucose	IEA	biological_process
GO:0009898	Cytoplasmic side of plasma membrane	IDA	cellular_component
GO:0010043	Response to zinc ion	IEA	biological_process
GO:0010975	Regulation of neuron projection development	ISS	biological_process
GO:0010997	Anaphase-promoting complex binding	IPI	molecular_function
GO:0014067	Negative regulation of phosphatidylinositol 3-kinase signaling	TAS	biological_process
GO:0016314	Phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase activity	IDA TAS	molecular_function
GO:0016477	Cell migration	ISS	biological_process
GO:0016605	PML body	IEA	cellular_component
GO:0019899	Enzyme binding	IPI	molecular_function
GO:0019901	Protein kinase binding	IEA	molecular_function
GO:0021542	Dentate gyrus development	ISS	biological_process
GO:0021955	Central nervous system neuron axonogenesis	ISS	biological_process
GO:0030165	PDZ domain binding	IPI	molecular_function
GO:0030336	Negative regulation of cell migration	IMP	biological_process
GO:0031642	Negative regulation of myelination	IEA	biological_process
GO:0031647	Regulation of protein stability	IMP	biological_process
GO:0031658	Negative regulation of cyclin-dependent protein serine/threonine kinase activity involved in G1/S transition of mitotic cell cycle	IDA	biological_process
GO:0032286	Central nervous system myelin maintenance	ISS	biological_process
GO:0032355	Response to estradiol	IEA	biological_process
GO:0032535	Regulation of cellular component size	ISS	biological_process
GO:0033032	Regulation of myeloid cell apoptotic process	IEA	biological_process
GO:0033198	Response to ATP	IEA	biological_process
GO:0033555	Multicellular organismal response to stress	ISS	biological_process
GO:0035176	Social behavior	ISS	biological_process
GO:0035335	Peptidyl-tyrosine dephosphorylation	IDA	biological_process
GO:0035749	Myelin sheath adaxonal region	ISS	cellular_component
GO:0038095	Fc-epsilon receptor signaling pathway	TAS	biological_process
GO:0042493	Response to drug	IEA	biological_process
GO:0042711	Maternal behavior	IEA	biological_process
GO:0042995	Cell projection	IDA	cellular_component
GO:0043005	Neuron projection	ISS	cellular_component
GO:0043065	Positive regulation of apoptotic process	IEA	biological_process
GO:0043066	Negative regulation of apoptotic process	IEA	biological_process
GO:0043197	Dendritic spine	IEA	cellular_component
GO:0043220	Schmidt-Lanterman incisure	ISS	cellular_component
GO:0043491	Protein kinase B signaling	ISS	biological_process
GO:0043542	Endothelial cell migration	IEA	biological_process
GO:0043647	Inositol phosphate metabolic process	TAS	biological_process
GO:0044281	Small molecule metabolic process	TAS	biological_process
GO:0045087	Innate immune response	TAS	biological_process
GO:0045211	Postsynaptic membrane	IEA	cellular_component
GO:0045471	Response to ethanol	IEA	biological_process
GO:0045475	Locomotor rhythm	ISS	biological_process
GO:0045792	Negative regulation of cell size	ISS	biological_process
GO:0046621	Negative regulation of organ growth	ISS	biological_process
GO:0046685	Response to arsenic-containing substance	IEA	biological_process
GO:0046855	Inositol phosphate dephosphorylation	IDA	biological_process
GO:0046856	Phosphatidylinositol dephosphorylation	IDA IMP	biological_process
GO:0048008	Platelet-derived growth factor receptor signaling pathway	IEA	biological_process
GO:0048011	Neurotrophin TRK receptor signaling pathway	TAS	biological_process
GO:0048015	Phosphatidylinositol-mediated signaling	TAS	biological_process
GO:0048738	Cardiac muscle tissue development	IEA	biological_process
GO:0048853	Forebrain morphogenesis	ISS	biological_process
GO:0048854	Brain morphogenesis	ISS	biological_process
GO:0050680	Negative regulation of epithelial cell proliferation	IEA	biological_process
GO:0050765	Negative regulation of phagocytosis	IEA	biological_process
GO:0050771	Negative regulation of axonogenesis	ISS	biological_process
GO:0050821	Protein stabilization	IDA	biological_process
GO:0050852	T cell receptor signaling pathway	TAS	biological_process
GO:0051091	Positive regulation of sequence-specific DNA binding transcription factor activity	IMP	biological_process
GO:0051717	Inositol-1,3,4,5-tetrakisphosphate 3-phosphatase activity	IDA TAS	molecular_function
GO:0051800	Phosphatidylinositol-3,4-bisphosphate 3-phosphatase activity	IDA TAS	molecular_function
GO:0051895	Negative regulation of focal adhesion assembly	IMP	biological_process
GO:0051898	Negative regulation of protein kinase B signaling	IMP	biological_process
GO:0060024	Rhythmic synaptic transmission	ISS	biological_process
GO:0060070	Canonical Wnt signaling pathway	IDA	biological_process
GO:0060074	Synapse maturation	ISS	biological_process
GO:0060134	Prepulse inhibition	ISS	biological_process
GO:0060179	Male mating behavior	IEA	biological_process
GO:0060291	Long-term synaptic potentiation	IEA	biological_process
GO:0060292	Long term synaptic depression	IEA	biological_process
GO:0060736	Prostate gland growth	IEA	biological_process
GO:0060997	Dendritic spine morphogenesis	ISS	biological_process
GO:0061002	Negative regulation of dendritic spine morphogenesis	ISS	biological_process
GO:0090071	Negative regulation of ribosome biogenesis	IEA	biological_process
GO:0090344	Negative regulation of cell aging	IEA	biological_process
GO:0090394	Negative regulation of excitatory postsynaptic membrane potential	ISS	biological_process
GO:0097105	Presynaptic membrane assembly	ISS	biological_process
GO:0097107	Postsynaptic density assembly	ISS	biological_process
GO:2000060	Positive regulation of protein ubiquitination involved in ubiquitin-dependent protein catabolic process	IDA	biological_process
GO:2000134	Negative regulation of G1/S transition of mitotic cell cycle	IDA	biological_process
GO:2000463	Positive regulation of excitatory postsynaptic membrane potential	ISS	biological_process
GO:2000808	Negative regulation of synaptic vesicle clustering	ISS	biological_process
GO:2001235	Positive regulation of apoptotic signaling pathway	IEA	biological_process

Entries Per Page

Displaying Page of

4. Expression levels in datasets

Meta-analysis result

p-value up	p-value down	FDR up	FDR down
0.9364409521	0.1028444436	0.9999902473	0.6145636034

Individual experiment result
( "-" represent NA in the specific microarray platform )

Data source	Up or down	Log fold change
GSE11954	Down	-0.3533409490
GSE13712_SHEAR	Down	-0.1818629570
GSE13712_STATIC	Down	-0.0751387870
GSE19018	Up	0.3068970661
GSE19899_A1	Up	0.0816024256
GSE19899_A2	Down	-0.3898145693
PubMed_21979375_A1	Down	-0.4549896670
PubMed_21979375_A2	Down	-0.2228952510
GSE35957	Down	-0.0604933483
GSE36640	Up	0.0021209995
GSE54402	Down	-0.3217979059
GSE9593	Down	-0.3791067601
GSE43922	Down	-0.1819040012
GSE24585	Down	-0.2274741276
GSE37065	Down	-0.0826974624
GSE28863_A1	Up	0.2845922839
GSE28863_A2	Down	-0.0432316668
GSE28863_A3	Down	-0.1488636466
GSE28863_A4	Up	0.0682920488
GSE48662	Up	0.2235580291

5. Regulation relationships with compounds/drugs/microRNAs

Compounds

Not regulated by compounds

Drugs

Not regulated by drugs

MicroRNAs

mirTarBase

MiRNA_name	mirBase ID	miRTarBase ID	Experiment	Support type	References (Pubmed ID)
hsa-miR-17-5p	MIMAT0000070	MIRT000499	Luciferase reporter assay//Western blot	Functional MTI	20227518
hsa-miR-17-5p	MIMAT0000070	MIRT000499	Luciferase reporter assay//qRT-PCR//Western blot	Non-Functional MTI	20008935
hsa-miR-17-5p	MIMAT0000070	MIRT000499	Luciferase reporter assay	Functional MTI	21283765
hsa-miR-17-5p	MIMAT0000070	MIRT000499	Luciferase reporter assay	Functional MTI	23418359
hsa-miR-217	MIMAT0000274	MIRT000533	Luciferase reporter assay//Western blot	Functional MTI	20216554
hsa-miR-217	MIMAT0000274	MIRT000533	Luciferase reporter assay	Functional MTI	23471579
hsa-miR-216a-5p	MIMAT0000273	MIRT000534	Luciferase reporter assay//Western blot	Functional MTI	20216554
hsa-miR-216a-5p	MIMAT0000273	MIRT000534	Luciferase reporter assay	Functional MTI	23471579
hsa-miR-214-3p	MIMAT0000271	MIRT000799	Western blot//qRT-PCR//Luciferase reporter assay//Reporter assay;Other	Functional MTI	18199536
hsa-miR-214-3p	MIMAT0000271	MIRT000799	Luciferase reporter assay//Microarray//qRT-PCR//Western blot	Functional MTI	20548023
hsa-miR-214-3p	MIMAT0000271	MIRT000799	Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	21228352
hsa-miR-26a-5p	MIMAT0000082	MIRT001095	Western blot//Luciferase reporter assay	Functional MTI	19487573
hsa-miR-26a-5p	MIMAT0000082	MIRT001095	Luciferase reporter assay//Western blot	Functional MTI	20216554
hsa-miR-26a-5p	MIMAT0000082	MIRT001095	GFP reporter assay//Luciferase reporter assay//Western blot	Functional MTI	20080666
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Western blot	Functional MTI	19672202
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay	Functional MTI	19072831
hsa-miR-21-5p	MIMAT0000076	MIRT001190	qRT-PCR//Western blot	Functional MTI	19906824
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	18850008
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Western blot	Functional MTI	20216554
hsa-miR-21-5p	MIMAT0000076	MIRT001190	qRT-PCR//Luciferase reporter assay//Western blot	Functional MTI	20223231
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Microarray//immunohistochemistry	Functional MTI (Weak)	19175831
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay//Western blot//Reporter assay;Western blot;Microarray	Functional MTI	20048743
hsa-miR-21-5p	MIMAT0000076	MIRT001190	qRT-PCR//Western blot	Functional MTI	20813833
hsa-miR-21-5p	MIMAT0000076	MIRT001190	GFP reporter assay//Northern blot//qRT-PCR//Western blot//ASO assay	Functional MTI	19641183
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay	Functional MTI	19253296
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Immunocytochemistry//Luciferase reporter assay//Northern blot//qRT-PCR//Western blot//Microarray//Reporter assay	Functional MTI	17681183
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Northern blot//qRT-PCR//Western blot//Reporter assay	Functional MTI	16762633
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay//qRT-PCR	Functional MTI	20797623
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Immunohistochemistry//qRT-PCR//Western blot	Functional MTI	20978511
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay//Western blot	Functional MTI	22267008
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Immunohistochemistry	Non-Functional MTI (Weak)	19473551
hsa-miR-21-5p	MIMAT0000076	MIRT001190	ELISA//Immunoblot//qRT-PCR	Functional MTI (Weak)	22678116
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay	Functional MTI	22956424
hsa-miR-21-5p	MIMAT0000076	MIRT001190	qRT-PCR//Western blot	Functional MTI	22761812
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Immunohistochemistry//Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	22770403
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay//Western blot	Functional MTI	22879939
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Luciferase reporter assay	Functional MTI	23226804
hsa-miR-21-5p	MIMAT0000076	MIRT001190	Western blot	Functional MTI	21544242
hsa-miR-494-3p	MIMAT0002816	MIRT001209	qRT-PCR//Luciferase reporter assay//Western blot	Functional MTI	20006626
hsa-miR-494-3p	MIMAT0002816	MIRT001209	Flow//Luciferase reporter assay//Microarray//qRT-PCR//Western blot	Functional MTI	22544933
hsa-miR-519a-3p	MIMAT0002869	MIRT006233	Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	22262409
hsa-miR-519d-3p	MIMAT0002853	MIRT006196	Luciferase reporter assay//Western blot	Functional MTI	22262409
hsa-miR-29b-3p	MIMAT0000100	MIRT006098	Western blot;Microarray;Other	Functional MTI	21359530
hsa-miR-19a-3p	MIMAT0000073	MIRT002958	qRT-PCR//Western blot	Functional MTI	18460397
hsa-miR-19a-3p	MIMAT0000073	MIRT002958	Luciferase reporter assay//Reporter assay	Functional MTI	14697198
hsa-miR-19a-3p	MIMAT0000073	MIRT002958	Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	21853360
hsa-miR-141-3p	MIMAT0000432	MIRT003281	Luciferase reporter assay//Western blot//Reporter assay;Western blot;Other	Functional MTI	20053927
hsa-miR-19b-3p	MIMAT0000074	MIRT003371	Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	20008935
hsa-miR-18a-5p	MIMAT0000072	MIRT003370	Luciferase reporter assay//qRT-PCR//Western blot	Non-Functional MTI	20008935
hsa-miR-20a-5p	MIMAT0000075	MIRT003369	Luciferase reporter assay//qRT-PCR//Western blot	Non-Functional MTI	20008935
hsa-miR-20a-5p	MIMAT0000075	MIRT003369	Luciferase reporter assay	Functional MTI	21283765
hsa-miR-221-3p	MIMAT0000278	MIRT005585	FACS//Flow//Luciferase reporter assay//Northern blot//Western blot	Functional MTI	20618998
hsa-miR-221-3p	MIMAT0000278	MIRT005585	Flow//Immunohistochemistry//Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	19962668
hsa-miR-221-3p	MIMAT0000278	MIRT005585	Luciferase reporter assay	Functional MTI	23372675
hsa-miR-222-3p	MIMAT0000279	MIRT005586	FACS//Flow//Luciferase reporter assay//Northern blot//Western blot	Functional MTI	20618998
hsa-miR-222-3p	MIMAT0000279	MIRT005586	Flow//Immunohistochemistry//Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	19962668
hsa-miR-222-3p	MIMAT0000279	MIRT005586	Western blot	Functional MTI	23028614
hsa-miR-106b-5p	MIMAT0000680	MIRT005865	Luciferase reporter assay	Functional MTI	21283765
hsa-miR-93-5p	MIMAT0000093	MIRT006216	GFP reporter assay//qRT-PCR//Western blot	Functional MTI	22465665
hsa-miR-519c-3p	MIMAT0002832	MIRT006640	Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	22262409
hsa-miR-103a-3p	MIMAT0000101	MIRT006693	Western blot	Non-Functional MTI	22593189
hsa-miR-107	MIMAT0000104	MIRT006694	Western blot	Non-Functional MTI	22593189
hsa-miR-23a-3p	MIMAT0000078	MIRT006987	Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	23019365
hsa-miR-29a-3p	MIMAT0000086	MIRT007028	Luciferase reporter assay//Reporter assay	Functional MTI	21573166
hsa-miR-29a-3p	MIMAT0000086	MIRT007028	Luciferase reporter assay	Functional MTI	23426367
hsa-miR-23b-3p	MIMAT0000418	MIRT007096	Luciferase reporter assay	Functional MTI	23189187
hsa-miR-144-3p	MIMAT0000436	MIRT007190	Immunoprecipitaion//Luciferase reporter assay//qRT-PCR//Western blot	Functional MTI	23125220
hsa-miR-193b-3p	MIMAT0002819	MIRT041436	CLASH	Functional MTI (Weak)	23622248
hsa-miR-181b-5p	MIMAT0000257	MIRT047231	CLASH	Functional MTI (Weak)	23622248

Entries Per Page

Displaying Page of

mirRecord

MicroRNA name	mirBase ID	Target site number	MiRNA mature ID	Test method inter	MiRNA regulation site	Pubmed ID
hsa-miR-19a-3p	MIMAT0000073	2	hsa-miR-19a			14697198
hsa-miR-19a-3p	MIMAT0000073	1	hsa-miR-19a			14697198
hsa-miR-19a-3p	MIMAT0000073	3	hsa-miR-19a			14697198
hsa-miR-214-3p	MIMAT0000271	1	hsa-miR-214	{Western blot}{Western blot}	{overexpression}{underexpression by 2'-O-Me antisense miRNA oligonucleotides}	18199536
hsa-miR-22-3p	MIMAT0000077	NA	hsa-miR-22	{Western blot}	{overexpression by miRNA precursor transfection}	0
hsa-miR-21-5p	MIMAT0000076	NA	hsa-miR-21	{Western blot}	{overexpression by miRNA precursor transfection}	19906824
hsa-miR-222-3p	MIMAT0000279	NA	hsa-miR-222	{Western blot}	{downregulation by anti-miRNA}	20618998
hsa-miR-221-3p	MIMAT0000278	NA	hsa-miR-221	{Western blot}	{downregulation by anti-miRNA}	20618998
hsa-miR-29a-3p	MIMAT0000086	1	hsa-miR-29a	{Western blot}	{overexpression by miRNA precursor transfection}	21573166
hsa-miR-29a-3p	MIMAT0000086	2	hsa-miR-29a	{Western blot}	{overexpression by miRNA precursor transfection}	21573166

Entries Per Page

Displaying Page of

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 43 abstracts the gene occurs.

PubMed ID of the article	Sentenece the gene occurs
28003865	These data indicate that the signal pathway to ROS generation in replicative aged skin cells can be stimulated by reduced PTEN level
27009837	These results suggest that Ad-Bmi-1i not only inhibits tumor growth and stem cell-like phenotype by inducing cellular senescence directly, but also has an indirect anti-tumor activity by anti-angiogenesis effects via regulating PTEN/AKT/VEGF pathway
26686419	We previously showed that CSIG plays an important role in regulating cell proliferation and cellular senescence progression through inhibiting PTEN, however, which domain or region of CSIG contributes to this function
26686419	The data showed that expression of CSIG potently reduced PTEN expression, increased cell proliferation rates, and reduced the senescent phenotype (lower SA-beta-gal activity)
26686419	By contrast, neither the expression of CSIG N- terminal (NT) fragment containing the ribosomal L1 domain nor C-terminal (CT) fragment containing Lys-rich region could significantly altered the levels of PTEN; instead of promoting cell proliferation and delaying cellular senescence, expression of CSIG-NT or CSIG-CT inhibited cell proliferation and accelerated cell senescence (increased SA-beta-gal activity) compared to either CSIG over-expressing or control (empty vector transfected) cells
26655726	The PTEN tumor suppressor gene and its role in lymphoma pathogenesis
26655726	The phosphatase and tensin homolog gene PTEN is one of the most frequently mutated tumor suppressor genes in human cancer
26655726	Loss of PTEN function occurs in a variety of human cancers via its mutation, deletion, transcriptional silencing, or protein instability
26655726	PTEN deficiency in cancer has been associated with advanced disease, chemotherapy resistance, and poor survival
26655726	In addition to having lipid phosphorylation activity, PTEN has critical roles in the regulation of genomic instability, DNA repair, stem cell self-renewal, cellular senescence, and cell migration
26655726	Although PTEN deficiency in solid tumors has been studied extensively, rare studies have investigated PTEN alteration in lymphoid malignancies
26655726	However, genomic or epigenomic aberrations of PTEN and dysregulated signaling are likely critical in lymphoma pathogenesis and progression
26655726	This review provides updated summary on the role of PTEN deficiency in human cancers, specifically in lymphoid malignancies; the molecular mechanisms of PTEN regulation; and the distinct functions of nuclear PTEN
26655726	Therapeutic strategies for rescuing PTEN deficiency in human cancers are proposed
26511486	Given that human prostate cancer arises from precancerous lesions such as high-grade prostatic intraepithelial neoplasia (HG-PIN), which frequently have lost phosphatase and tensin homolog (PTEN) tumor suppressor permitting phosphatidylinositol-3-OH kinase (PI3K)-protein kinase B (AKT) oncogenic signaling, we tested the efficacy of MSeA to inhibit HG-PIN progression in Pten prostate-specific knockout (KO) mice and assessed the mechanistic involvement of p53-mediated cellular senescence and of the androgen receptor (AR)
26511486	We observed that short-term (4 weeks) oral MSeA treatment significantly increased expression of P53 and P21Cip1 proteins and senescence-associated-beta-galactosidase staining, and reduced Ki67 cell proliferation index in Pten KO prostate epithelium
26511486	Long-term (25 weeks) MSeA administration significantly suppressed HG-PIN phenotype, tumor weight, and prevented emergence of invasive carcinoma in Pten KO mice
26511486	Mechanistically, the long-term MSeA treatment not only sustained P53-mediated senescence, but also markedly reduced AKT phosphorylation and AR abundance in the Pten KO prostate
26477312	NFATc1 promotes prostate tumorigenesis and overcomes PTEN loss-induced senescence
26477312	To further characterize interactions between genes involved in prostate tumorigenesis, we generated mice with both NFATc1 activation and Pten inactivation in prostate
26477312	We showed that NFATc1 activation led to acceleration of Pten null-driven prostate tumorigenesis by overcoming the PTEN loss-induced cellular senescence through inhibition of p21 activation
26085373	Mechanistically, we show that Pten loss increases CK2 levels by activating STAT3
26085373	CK2 upregulation in Pten null tumours affects the stability of Pml, an essential regulator of senescence
26085373	However, CK2 inhibition stabilizes Pml levels enhancing senescence in Pten null tumours
25328137	Despite NR2E1 regulating targets like p21(CIP1) or PTEN we still lack a full explanation for its role in NSC self-renewal and tumorigenesis
25156255	Here we show that at the onset of senescence, PTEN null prostate tumours in mice are massively infiltrated by a population of CD11b(+)Gr-1(+) myeloid cells that protect a fraction of proliferating tumour cells from senescence, thus sustaining tumour growth
24866151	Loss of the PTEN and TP53 tumor suppressor genes is commonly observed in prostate cancer, whereas their compound loss is often observed in advanced prostate cancer
24866151	Surprisingly, we also find that PARP-induced cellular senescence is morphed into an apoptotic response upon compound loss of PTEN and p53
24782600	Activation of egr-1, in turn, upregulates the dual specificity phosphatase, phosphatase and tensin homologue deleted on chromosome ten (PTEN) resulting in activation of pro-apoptotic caspase-3 and caspase-9 and reduced expression of the anti-apoptosis protein, survivin
24782600	This paradigm has human relevance since increased expression of PTEN and reduced expression of survivin were demonstrated in gastric mucosa of aging individuals
24704020	Prognostic significance of biallelic loss of PTEN in clear cell renal cell carcinoma
24704020	PURPOSE: We investigated the clinical implications of biallelic loss of PTEN in clear cell renal cell carcinoma and whether PTEN biallelic loss would induce p53 dependent cellular senescence
24704020	PTEN allelic status was classified into 3 groups, including biallelic PTEN loss (homozygous deletion or combined heterozygous deletion and mutation), monoallelic PTEN loss (heterozygous deletion or mutation) and absent allelic loss
24704020	6%) had biallelic PTEN loss and 69 (16
24704020	PTEN allelic loss was associated with late tumor stage and high histological grade
24704020	About half of the patients with PTEN biallelic loss had accompanying TP53 allelic loss
24704020	Biallelic loss of PTEN did not increase the expression of genes related to p53 dependent cellular senescence
24704020	CONCLUSIONS: PTEN biallelic loss may be a prognostic marker for clear cell renal cell carcinoma
24270409	Although such 'escape' from senescence is not sufficient to promote thyroid tumorigenesis in adult mice up to 5 months, the onset of Phosphatase and tensin homolog (Pten)-induced tumor formation is accelerated when Spry1 is concomitantly eliminated
24074787	The timing of TP53 mutation also depends on the tumor subtype, being the first important event in luminal tumors but occurring after PTEN loss in basal-like tumors
24052415	The expression of p16 and PTEN do not seem to cause synergism of senescence in the benign lesions analyzed in p21p27 double-KO mice
23936028	Using the conditional PTEN deletion mouse model, we previously reported that survivin levels increase with prostate tumor growth
23936028	We then serially, from about 10-56 weeks of age, evaluated histopathologic changes in the prostate of mice with PTEN deletion combined with survivin mono- or bi-allelic gene deletion
23936028	A reduced proliferation index as well as apoptotic and senescent cells were detected in the lesions of mice with compound PTEN/survivin deficiency throughout the time points examined
23904845	No pathogenetic mutations in CDKN2A, BRAF, NRAS, KRAS, cKIT, TP53 and PTEN genes were observed
23826727	In this model, PTEN loss prevents the decline in proliferation capacity in aged beta-cells and restores the ability of aged beta-cells to respond to injury-induced regeneration
23826727	Using several animal and cell models where we can manipulate PTEN expression, we found that PTEN blocks cell cycle re-entry through a novel pathway leading to an increase in p16(ink4a), a cell cycle inhibitor characterized for its role in cellular senescence/aging
23826727	A downregulation in p16(ink4a) occurs when PTEN is lost as a result of cyclin D1 induction and the activation of E2F transcription factors
23727861	Prostate-specific inactivation of Zbtb7a leads to a marked acceleration of Pten loss-driven prostate tumorigenesis through bypass of Pten loss-induced cellular senescence (PICS)
23535008	Therefore, we investigated the role of gene silencing (DNA promoter methylation of LINE-1, PTEN), genetic aberrations (karyotype, KRAS and BRAF mutations) as well as their contribution to the proliferation rate and migratory potential that underlies "initial" and "final" passage sarcoma cells
23535008	Increased proliferative potential of final passage STS cells was not associated with significant differences in methylation (LINE-1, PTEN) and mutation status (KRAS, BRAF), but it was dependent on the amount of chromosomal aberrations
22836754	B-Raf activation cooperates with PTEN loss to drive c-Myc expression in advanced prostate cancer
22652801	Oncogene induced CS can be promoted by the loss of tumor suppressor genes, such as PTEN
22253608	Cytoplasmic polyadenylation element binding protein deficiency stimulates PTEN and Stat3 mRNA translation and induces hepatic insulin resistance
22253608	An investigation of Cpeb1 knockout mice revealed that the expression of two particular negative regulators of insulin action, PTEN and Stat3, were aberrantly increased
22253608	Analysis of HepG2 cells, a human liver cell line, depleted of CPEB demonstrated that this protein directly regulates the translation of PTEN and Stat3 mRNAs
22120720	This phenomenon was not restricted to breast cancer cells, as it was also seen in glioblastoma cells in which PKCiota is activated by loss of PTEN
22037217	Loss of TGF-beta signaling and PTEN promotes head and neck squamous cell carcinoma through cellular senescence evasion and cancer-related inflammation
21930937	HER2 overcomes PTEN (loss)-induced senescence to cause aggressive prostate cancer
21930937	In this study, we show that patients who develop prostate tumors with low levels of PTEN and high levels of HER2/3 have a poor prognosis
21930937	This is functionally relevant, as targeting Her2 activation to the murine prostate cooperates with Pten loss and drives CaP progression
21930937	Taken together, these data suggest that stratification of CaP patients for HER2/3 and PTEN status could identify patients with aggressive CaP who may respond favorably to MEK inhibition
21909130	Furthermore, our data imply that chronic activation of AKT signalling provides selective pressure for the loss of p53 function, consistent with observations that PTEN or PIK3CA mutations are significantly associated with p53 mutation in a number of human tumour types
21695255	Mammalian target of rapamycin is a therapeutic target for murine ovarian endometrioid adenocarcinomas with dysregulated Wnt/beta-catenin and PTEN
21695255	However, the role of WNT/beta-catenin and PTEN/AKT signaling in the etiology and/or progression of this disease is currently unclear
21695255	Combining dysregulated beta-catenin with homozygous deletion of PTEN in the OSE resulted in development of significantly more aggressive tumors, which was correlated with inhibition of p53 expression and cellular senescence
21695255	Ectopic allotransplants of the mouse ovarian tumor cells with a gain-of-function mutation in beta-catenin and PTEN deletion developed into tumors with OEA histology, the growth of which were significantly inhibited by oral rapamycin treatment
21695255	These studies demonstrate that rapamycin might be an effective therapeutic for human ovarian endometrioid patients with dysregulated Wnt/beta-catenin and Pten/PI3K signaling
21594579	Induction of cellular senescence by oncogenic insults, such as Ras overexpression or by inactivation of PTEN tumor suppressor, triggers an ARF/p53-dependent tumor-suppressive effect which can significantly restrict cancer progression
21286718	The combination could also inhibit the expression of Cyclin D1 and phosphorylated mTOR while had no impact on p53, p16, PTEN, and HIF-1alpha
21241890	Nuclear PTEN regulates the APC-CDH1 tumor-suppressive complex in a phosphatase-independent manner
21241890	Recently, nuclear compartmentalization of PTEN was found as a key component of its tumor-suppressive activity; however its nuclear function remains poorly defined
21241890	Here we show that nuclear PTEN interacts with APC/C, promotes APC/C association with CDH1, and thereby enhances the tumor-suppressive activity of the APC-CDH1 complex
21241890	We find that nuclear exclusion but not phosphatase inactivation of PTEN impairs APC-CDH1
21241890	This nuclear function of PTEN provides a straightforward mechanistic explanation for the fail-safe cellular senescence response elicited by acute PTEN loss and the tumor-suppressive activity of catalytically inactive PTEN
21241890	Importantly, we demonstrate that PTEN mutant and PTEN null states are not synonymous as they are differentially sensitive to pharmacological inhibition of APC-CDH1 targets such as PLK1 and Aurora kinases
20938386	Total RNA isolated from these samples was used to measure the gene expression of p16INK4a, RB, cyclin D1, CDK4, PTEN, p27KIP, p19ARF, p21, TERT, and RAGE by real-time polymerase chain reaction assay
20938386	The mRNA levels of p16INK4a, RB, PTEN, p27KIP, p19ARF, and RAGE were upregulated
20622047	In addition to the canonical function of dephosphorylation of phosphatidylinositol-3,4,5-trisphosphate (PIP3), recent studies showed the intriguing roles of PTEN in regulating genomic instability, DNA repair, stem cell self-renewal, cellular senescence, and cell migration and/or metastasis
20622047	Clinically, PTEN mutations and deficiencies are prevalent in many types of human cancers
20622047	Severe PTEN deficiency is also associated with advanced tumor stage and therapeutic resistance, such as the resistance to trastuzumab, an anti-HER2 therapy
20622047	In this review, we highlight our current knowledge of PTEN function and the recent discoveries in dissecting the PTEN signaling pathway
20197621	We previously demonstrated in a mouse model of prostate cancer that inactivation of the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (Pten) elicits a senescence response that opposes tumorigenesis
20197621	Using mouse embryonic fibroblasts, we determined that PICS occurs rapidly after Pten inactivation, in the absence of cellular proliferation and DDR
20197621	Importantly, we demonstrated that pharmacological inhibition of PTEN drives senescence and inhibits tumorigenesis in vivo in a human xenograft model of prostate cancer
20174572	Elevated expression of AKT has been noted in a significant percentage of primary human breast cancers, mainly as a consequence of the PTEN/PI3K pathway deregulation
19690330	Acute loss of Pten leads to an increase in the abundance of p19(Arf), p53, and p21 proteins as part of a fail-safe senescence response
19690330	In both prostate epithelium and primary mouse embryo fibroblasts (MEFs), the increase in p53 protein abundance found upon loss of Pten was unaffected by the simultaneous loss of p19(Arf)
19690330	Consistent with the effect of p19(Arf) loss in Pten-deficient mouse prostate, we found that in human prostate cancers, loss of PTEN was not associated with loss of p14(ARF) (the human equivalent of mouse p19(Arf))
19690330	Collectively, these data reveal differential consequences of p19(Arf) inactivation in prostate cancer and MEFs upon Pten loss that are independent of the p53 pathway
19647222	We report that knocking down the expression of inositol polyphosphate 4-phosphatase type II (INPP4B) in human epithelial cells, like knockdown of PTEN, resulted in enhanced Akt activation and anchorage-independent growth and enhanced overall motility
19647222	Dual knockdown of INPP4B and PTEN resulted in cellular senescence
18765664	S1P-induced Akt and ERK1/2 activation were comparable between ECs of different in vitro ages; however, PTEN (phosphatase and tensin homolog deleted on chromosome 10) activity was significantly elevated and Rac activation was inhibited in senescent ECs
18765664	Rac activation and senescent-associated impairments were restored in senescent ECs by the expression of dominant-negative PTEN and by knocking down S1P(2) receptors
18765664	These results indicate that the impairment of function in senescent ECs in culture is mediated by an increase in S1P signaling through S1P(2)-mediated activation of the lipid phosphatase PTEN
18678645	CSIG inhibits PTEN translation in replicative senescence
18678645	Instead, CSIG negatively regulated PTEN and p27(Kip1) expressions, in turn promoting cell proliferation
18678645	In PTEN-silenced HEK 293 cells and PTEN-deficient human glioblastoma U87MG cells, the effect of CSIG on p27(Kip1) expression and cell division was abolished, suggesting that PTEN was required for the role of CSIG on p27(Kip1) regulation and cell cycle progression
18678645	Investigation into the underlying mechanism revealed that the regulation of PTEN by CSIG was achieved through a translational suppression mechanism
18678645	Knockdown of PTEN diminished the effect of CSIG on cellular senescence
18678645	Our findings indicate that CSIG acts as a novel regulatory component of replicative senescence, which requires PTEN as a mediator and involves in a translational regulatory mechanism
18577387	We propose a stochastic model of p53 regulation, which is based on two feedback loops: the negative, coupling p53 with its immediate downregulator Mdm2, and the positive, which involves PTEN, PIP3 and Akt
18353141	Loci with established importance in melanoma, like CDKN2A, BRAF and PTEN, have been joined by some less familiar genes including transcription factor sequences TBX2 and STK11 (LKB)
16079851	The PTEN and p53 tumour suppressors are among the most commonly inactivated or mutated genes in human cancer including prostate cancer
16079851	Although they are functionally distinct, reciprocal cooperation has been proposed, as PTEN is thought to regulate p53 stability, and p53 to enhance PTEN transcription
16079851	Here we show that conditional inactivation of Trp53 in the mouse prostate fails to produce a tumour phenotype, whereas complete Pten inactivation in the prostate triggers non-lethal invasive prostate cancer after long latency
16079851	Strikingly, combined inactivation of Pten and Trp53 elicits invasive prostate cancer as early as 2 weeks after puberty and is invariably lethal by 7 months of age
16079851	Importantly, acute Pten inactivation induces growth arrest through the p53-dependent cellular senescence pathway both in vitro and in vivo, which can be fully rescued by combined loss of Trp53
10832053	In this review, we describe three senescence-inducing pathways involving these inhibitors, namely, the p16(INK4a)/Rb pathway, the p19(ARF)/p53/p21(Cip1) pathway, and the PTEN/p27(Kip1) pathway

Entries Per Page

Displaying Page of

Navigator

1.General information
2.Neighbors in the network
3.Gene Ontology Annotation
4.Expression levels
5.Regulation
6.Text-mining results

HCSGD entry for PTEN

1. General information

2. Neighbors in the network

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

4. Expression levels in datasets

Meta-analysis result

Individual experiment result ( "-" represent NA in the specific microarray platform )

( "-" represent NA in the specific microarray platform )

5. Regulation relationships with compounds/drugs/microRNAs

Compounds

Drugs

MicroRNAs

mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

mirRecord

MicroRNA name

mirBase ID

Target site number

MiRNA mature ID

Test method inter

MiRNA regulation site

Reporter target site

Pubmed ID

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 43 abstracts the gene occurs.

PubMed ID of the article

Sentenece the gene occurs

Navigator

Individual experiment result
( "-" represent NA in the specific microarray platform )