ArticleGenes & cancer2011
The Tumor Suppressor, p190RhoGAP, Differentially Initiates Apoptosis and Confers Docetaxel Sensitivity to Breast Cancer Cells.
Article in Genes & cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Rho GTPase-activating protein 35 rs1052667 polymorphism and osteosarcoma risk and prognosis.BioMed research international · 2014Trial
- The role of small GTPases in bisphenol AF-induced multinucleation in comparison with dibutyl phthalate in the male germ cells.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- p190RhoGAPs, theCells · 2019Review
- Regulation of Rho GTPase activity at the leading edge of migrating cells by p190RhoGAP.Small GTPases · 2019Review
- Genomic Comparison of Endometrioid Endometrial Carcinoma and Its Precancerous Lesions in Chinese Patients by High-Depth Next Generation Sequencing.Frontiers in oncology · 2019Article
- Bcl-2 inhibition sensitizes triple-negative human breast cancer cells to doxorubicin.Oncotarget · 2018Article
- Glucocorticoid receptor DNA binding factor 1 expression and osteosarcoma prognosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Bcl-2 family inhibition sensitizes human prostate cancer cells to docetaxel and promotes unexpected apoptosis under caspase-9 inhibition.Oncotarget · 2014Article
- Medroxyprogesterone acetate differentially regulates interleukin (IL)-12 and IL-10 in a human ectocervical epithelial cell line in a glucocorticoid receptor (GR)-dependent manner.The Journal of biological chemistry · 2014Article
- RhoA is down-regulated at cell-cell contacts via p190RhoGAP-B in response to tensional homeostasis.Molecular biology of the cell · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
p190RhoGAP (p190) is a negative regulator of RhoGTPases and a putative tumor suppressor, whose mechanism of tumor suppression is poorly defined. Ectopic expression of p190 induces various morphological phenotypes, including multinucleation, dendrite-like formation, and chromatin condensation, suggesting an involvement in apoptosis. We examined the possibility that p190 can function as a tumor suppressor by regulating induction of apoptosis. We show that the predominant phenotype of p190 overexpression in a variety of cell lines is apoptosis, which is mediated through p190's regulation of Rho and caspases. The secondary phenotypes, multinucleation and dendrite-like formation, are determined by transformation status, not cell lineage, and appear to be intermediate phenotypes in the p190-induced apoptotic pathway. Finally, we show that p190 levels can regulate the apoptotic response of breast cancer cell lines to docetaxel through its regulation of Rho. Together, these findings suggest that one mechanism by which p190 can mediate its tumor-suppressive function is through regulation of Rho-activated cell death pathways and that this function can be exploited to optimize the action of cytoskeletal-based chemotherapeutics, such as the taxanes.
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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.