ArticleProceedings of the National Academy of Sciences of the United States of America2005
Cellular transformation by the MSP58 oncogene is inhibited by its physical interaction with the PTEN tumor suppressor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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56 citing papers in PubMed, 116 citations in OpenAlex.
- Synthetic lethal approaches to target cancers with loss of PTEN function.Genes & diseases · 2023Article
- Inhibition of PI3K Signaling Intensified the Antileukemic Effects of Pioglitazone: New Insight into the Application of PPARγ Stimulators in Acute Lymphoblastic Leukemia.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023Article
- The impact of phosphorylated PTEN at threonine 366 on cortical connectivity and behaviour.Brain : a journal of neurology · 2022Article
- Redox regulation of tumor suppressor PTEN in cell signaling.Redox biology · 2020Review
- Role of Ubiquitination in PTEN Cellular Homeostasis and Its Implications in GB Drug Resistance.Frontiers in oncology · 2020Review
- PTEN Tumor-Suppressor: The Dam of Stemness in Cancer.Cancers · 2019Review
- Mps1 regulates spindle morphology through MCRS1 to promote chromosome alignment.Molecular biology of the cell · 2019Article
- PTEN-GSK3β-MOB1 axis controls neurite outgrowth in vitro and in vivo.Cellular and molecular life sciences : CMLS · 2018Article
- PTEN regulates glioblastoma oncogenesis through chromatin-associated complexes of DAXX and histone H3.3.Nature communications · 2017Article
- Correction of PTEN mutations in glioblastoma cell lines via AAV-mediated gene editing.PloS one · 2017Article
- MCRS1 associates with cytoplasmic dynein and mediates pericentrosomal material recruitment.Scientific reports · 2016Article
- The candidate oncogene (MCRS1) promotes the growth of human lung cancer cells via the miR-155-Rb1 pathway.Journal of experimental & clinical cancer research : CR · 2015Article
- Identification and characterization of nuclear and nucleolar localization signals in 58-kDa microspherule protein (MSP58).Journal of biomedical science · 2015Article
- PTEN induces apoptosis and cavitation via HIF-2-dependent Bnip3 upregulation during epithelial lumen formation.Cell death and differentiation · 2015Article
- PTEN: Multiple Functions in Human Malignant Tumors.Frontiers in oncology · 2015Review
- MCRS1 overexpression, which is specifically inhibited by miR-129*, promotes the epithelial-mesenchymal transition and metastasis in non-small cell lung cancer.Molecular cancer · 2014Article
- PTEN function: the long and the short of it.Trends in biochemical sciences · 2014Review
- PTEN, Longevity and Age-Related Diseases.Biomedicines · 2013Review
- Identification of PTEN at the ER and MAMs and its regulation of Ca(2+) signaling and apoptosis in a protein phosphatase-dependent manner.Cell death and differentiation · 2013Article
- Increased expression of the 58-kD microspherule protein (MSP58) is correlated with poor prognosis in glioma patients.Medical oncology (Northwood, London, England) · 2013Article
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5 authors at 1 institution in 1 country.
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Abstract
The PTEN (phosphatase and tensin homologue) tumor suppressor protein contains a single catalytic domain with both lipid and protein phosphatase activities. The remaining C-terminal half of the PTEN protein plays a role in its stability and is mutated in many clinical cancer samples. Here, we report that the PTEN C-terminal domain physically interacts with the forkhead-associated domain of the oncogenic MSP58 protein and that this interaction requires PTEN Thr-366. We further show that while MSP58 transforms Pten-/- mouse embryo fibroblasts (MEFs), concurrent introduction of wild-type PTEN causes a dramatic reduction in the number of MSP58-induced transformed foci. This PTEN-mediated inhibition of cellular transformation requires physical interaction as evidenced by the failure of PTEN(T366A) point mutation (residing within the MSP58 interaction domain) to suppress MSP-58-driven transformation. These observations, together with the capacity of catalytically inactive PTEN mutant (G129R) to suppress MSP58 oncogenicity, support the view that the C-terminal region of PTEN directly provides a previously uncharacterized biological function in its ability to regulate cellular transformation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.