ArticleMolecular cancer2013
PTEN suppresses the oncogenic function of AIB1 through decreasing its protein stability via mechanism involving Fbw7 alpha.
Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- FBXW7 in breast cancer: mechanism of action and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2023Review
- Targeting CDCP1 gene transcription coactivated by BRD4 and CBP/p300 in castration-resistant prostate cancer.Oncogene · 2022Article
- FBXW7: a critical tumor suppressor of human cancers.Molecular cancer · 2018Review
- Stanozolol administration combined with exercise leads to decreased telomerase activity possibly associated with liver aging.International journal of molecular medicine · 2018Article
- SYNJ2BP promotes the degradation of PTEN through the lysosome-pathway and enhances breast tumor metastasis via PI3K/AKT/SNAI1 signaling.Oncotarget · 2017Article
- NF-κB p65 Overexpression Promotes Bladder Cancer Cell Migration via FBW7-Mediated Degradation of RhoGDIα Protein.Neoplasia (New York, N.Y.) · 2017Article
- Sumoylation of TCF21 downregulates the transcriptional activity of estrogen receptor-alpha.Oncotarget · 2016Article
- Review
- PTEN stabilizes TOP2A and regulates the DNA decatenation.Scientific reports · 2015Article
- MicroRNA-17-5p induces drug resistance and invasion of ovarian carcinoma cells by targeting PTEN signaling.Journal of biological research (Thessalonike, Greece) · 2015Article
- DEC1 regulates breast cancer cell proliferation by stabilizing cyclin E protein and delays the progression of cell cycle S phase.Cell death & disease · 2015Article
- DACH1 inhibits SNAI1-mediated epithelial-mesenchymal transition and represses breast carcinoma metastasis.Oncogenesis · 2015Article
- FOXK2 transcription factor suppresses ERα-positive breast cancer cell growth through down-regulating the stability of ERα via mechanism involving BRCA1/BARD1.Scientific reports · 2015Article
- Focus on PTEN Regulation.Frontiers in oncology · 2015Review
- Association between EHBP1 rs721048(A>G) polymorphism and prostate cancer susceptibility: a meta-analysis of 17 studies involving 150,678 subjects.OncoTargets and therapy · 2015Article
- SUMOylation of GPS2 protein regulates its transcription-suppressing function.Molecular biology of the cell · 2014Article
- PTEN function: the long and the short of it.Trends in biochemical sciences · 2014Review
- Induction of the CLOCK gene by E2-ERα signaling promotes the proliferation of breast cancer cells.PloS one · 2014Article
- AIB1 cooperates with ERα to promote epithelial mesenchymal transition in breast cancer through SNAI1 activation.PloS one · 2013Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPhosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a phosphatase having both protein and lipid phosphatase activities, and is known to antagonize the phosphoinositide 3-kinase/AKT (PI3K/AKT) signaling pathway, resulting in tumor suppression. PTEN is also known to play a role in the regulation of numerous transcription factors. Amplified in breast cancer 1 (AIB1) is a transcriptional coactivator that mediates the transcriptional activities of nuclear receptors and other transcription factors. The present study investigated how PTEN may regulate AIB1, which is amplified and/or overexpressed in many human carcinomas, including breast cancers.
resultsPTEN interacted with AIB1 via its phophatase domain and regulated the transcriptional activity of AIB1 by enhancing the ubiquitin-mediated degradation of AIB1. This process did not appear to require the phosphatase activity of PTEN, but instead, involved the interaction between PTEN and F-box and WD repeat domain-containing 7 alpha (Fbw7α), the E3 ubiquitin ligase involved in the ubiquitination of AIB1. PTEN interacted with Fbw7α via its C2 domain, thereby acting as a bridge between AIB1 and Fbw7α, and this led to enhanced degradation of AIB1, which eventually accounted for its decreased transcriptional activity. At the cell level, knockdown of PTEN in MCF-7 cells promoted cell proliferation. However when AIB1 was also knocked down, knockdown of PTEN had no effect on cell proliferation.
conclusionsPTEN might act as a negative regulator of AIB1 whereby the association of PTEN with both AIB1 and Fbw7α could lead to the downregulation of AIB1 transcriptional activity, with the consequence of regulating the oncogenic function of AIB1.
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