ArticleCancer research2009
Overexpression of RhoA induces preneoplastic transformation of primary mammary epithelial cells.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
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- Establishment and characterization of immortalized sweat gland myoepithelial cells.Scientific reports · 2022Article
- Analysis ofOncology letters · 2021Article
- Gap Junctions and Wnt Signaling in the Mammary Gland: a Cross-Talk?Journal of mammary gland biology and neoplasia · 2019Review
- Nck deficiency is associated with delayed breast carcinoma progression and reduced metastasis.Molecular biology of the cell · 2017Article
- Nucleotide Dependent Switching in Rho GTPase: Conformational Heterogeneity and Competing Molecular Interactions.Scientific reports · 2017Article
- MiR-31 Regulates Rho-Associated Kinase-Myosin Light Chain (ROCK-MLC) Pathway and Inhibits Gastric Cancer Invasion: Roles of RhoA.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Inhibitors of Rho kinase (ROCK) signaling revert the malignant phenotype of breast cancer cells in 3D context.Oncotarget · 2016Article
- Phosphorylation and Activation of RhoA by ERK in Response to Epidermal Growth Factor Stimulation.PloS one · 2016Article
- Effect of RhoA gene silencing on proliferation and migration of gastric MGC-803 cells.International journal of clinical and experimental medicine · 2015Article
- Use of synthetic isoprenoids to target protein prenylation and Rho GTPases in breast cancer invasion.PloS one · 2014Article
- Characterization of cell lines derived from breast cancers and normal mammary tissues for the study of the intrinsic molecular subtypes.Breast cancer research and treatment · 2013Article
- Article
- PKC ε Phosphorylates and Mediates the Cell Membrane Localization of RhoA.ISRN oncology · 2013Article
- Nuclear expression of Rac1 in cervical premalignant lesions and cervical cancer cells.BMC cancer · 2012Article
- Haploinsufficiency in the prometastasis Kiss1 receptor Gpr54 delays breast tumor initiation, progression, and lung metastasis.Cancer research · 2011Article
- Proteomic identification of RhoA as a potential biomarker for proliferation and metastasis in hepatocellular carcinoma.Journal of molecular medicine (Berlin, Germany) · 2011Article
- A block in lineage differentiation of immortal human mammary stem / progenitor cells by ectopically-expressed oncogenes.Journal of carcinogenesis · 2011Article
- Breast cancer subtypes: two decades of journey from cell culture to patients.Advances in experimental medicine and biology · 2011Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Rho family small GTPases serve as molecular switches in the regulation of diverse cellular functions, including actin cytoskeleton remodeling, cell migration, gene transcription, and cell proliferation. Importantly, Rho overexpression is frequently seen in many carcinomas. However, published studies have almost invariably used immortal or tumorigenic cell lines to study Rho GTPase functions and there are no studies on the potential of Rho small GTPase to overcome senescence checkpoints and induce preneoplastic transformation of human mammary epithelial cells (hMEC). We show here that ectopic expression of wild-type (WT) RhoA as well as a constitutively active RhoA mutant (G14V) in two independent primary hMEC strains led to their immortalization and preneoplastic transformation. These cells have continued to grow over 300 population doublings (PD) with no signs of senescence, whereas cells expressing the vector or dominant-negative RhoA mutant (T19N) senesced after 20 PDs. Significantly, RhoA-T37A mutant, known to be incapable of interacting with many well-known Rho effectors including Rho kinase, PKN, mDia1, and mDia2, was also capable of immortalizing hMECs. Notably, similar to parental normal cells, Rho-immortalized cells have WT p53 and intact G(1) cell cycle arrest on Adriamycin treatment. Rho-immortalized cells were anchorage dependent and were unable to form tumors when implanted in nude mice. Lastly, microarray expression profiling of Rho-immortalized versus parental cells showed altered expression of several genes previously implicated in immortalization and breast cancer progression. Taken together, these results show that RhoA can induce the preneoplastic transformation of hMECs by altering multiple pathways linked to cellular transformation and breast cancer.
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Registered trials
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.