ArticleOncogene2004
Expression of activated M-Ras in a murine mammary epithelial cell line induces epithelial-mesenchymal transition and tumorigenesis.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Aberrant expression of MRAS and HEG1 as the biomarkers for osimertinib resistance in LUAD.Discover oncology · 2024Article
- Probing mutation-induced conformational transformation of the GTP/M-RAS complex through Gaussian accelerated molecular dynamics simulations.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Classical RAS proteins are not essential for paradoxical ERK activation induced by RAF inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Role of R-Ras Proteins in Normal and Pathologic Migration and Morphologic Change.The American journal of pathology · 2021Review
- Mechanisms and consequences of subcellular RNA localization across diverse cell types.Traffic (Copenhagen, Denmark) · 2020Review
- MRAS: A Close but Understudied Member of the RAS Family.Cold Spring Harbor perspectives in medicine · 2018Review
- RNA-sequencing reveals long-term effects of silver nanoparticles on human lung cells.Scientific reports · 2018Article
- Muscle RAS oncogene homolog (MRAS) recurrent mutation in Borrmann type IV gastric cancer.Cancer medicine · 2017Article
- A new role for the PI3K/Akt signaling pathway in the epithelial-mesenchymal transition.Cell adhesion & migration · 2015Review
- M-Ras induces Ral and JNK activation to regulate MEK/ERK-independent gene expression in MCF-7 breast cancer cells.Journal of cellular biochemistry · 2012Article
- Charting the NF-κB pathway interactome map.PloS one · 2012Article
- Targeting EGFR in Triple Negative Breast Cancer.Journal of Cancer · 2011Article
- Ras-association domain family 1C protein promotes breast cancer cell migration and attenuates apoptosis.BMC cancer · 2010Article
- Localized Rho GTPase activation regulates RNA dynamics and compartmentalization in tumor cell protrusions.The Journal of biological chemistry · 2008Article
- Restoration of E-cadherin cell-cell junctions requires both expression of E-cadherin and suppression of ERK MAP kinase activation in Ras-transformed breast epithelial cells.Neoplasia (New York, N.Y.) · 2008Article
- Characterization of R-ras3/m-ras null mice reveals a potential role in trophic factor signaling.Molecular and cellular biology · 2006Article
- Article
- Distinct molecular mechanisms underlying clinically relevant subtypes of breast cancer: gene expression analyses across three different platforms.BMC genomics · 2006Article
- Caveolin-1 deficiency (-/-) conveys premalignant alterations in mammary epithelia, with abnormal lumen formation, growth factor independence, and cell invasiveness.The American journal of pathology · 2006Article
- Epithelial-mesenchymal transition in development and cancer: role of phosphatidylinositol 3' kinase/AKT pathways.Oncogene · 2005Review
Corrections and comments
- Erratum issuedZhang, Kai-Xiu [corrected to Zhang, Kai-Xin]
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of activated mutants of M-Ras (G22V or Q71L), but not wild-type M-Ras, in a murine mammary epithelial cell line, scp2, resulted in epithelial-mesenchymal transition (EMT) and oncogenic transformation. Cells expressing constitutively active M-Ras continued to grow in the absence of serum and exhibited a loss of the epithelial markers cytokeratin, E-cadherin and beta-catenin, together with a gain of the mesenchymal marker vimentin, a loss of contact inhibition in monolayer growth and a gain of the capacity for anchorage-independent growth. Moreover, unlike the parental cells, they failed to form differentiated mammospheres on Matrigel and instead formed branched networks of cells that grew and invaded the Matrigel. The expression of activated p21 Ras (G12V H-Ras or Q61K N-Ras) also resulted in EMT and tumorigenesis, although there was evidence that expression of higher levels was toxic. Tumors derived from scp2 cells expressing activated M-Ras exhibited activation of Akt and of ERK. The levels of expression of Q71L M-Ras and G12V H-Ras required for tumorigenesis were comparable, although higher levels of the weaker G22V M-Ras mutant were selected for in vivo. These data indicate that the expression of activated mutants of M-Ras was sufficient for oncogenic transformation of a murine mammary epithelial cell line.
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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.