RhoC Induces Differential Expression of Genes Involved in Invasion and Metastasis in MCF10A Breast Cells
dc.contributor.author | Merajver, Sofia D. | en_US |
dc.contributor.author | Kumar-Sinha, Chandan | en_US |
dc.contributor.author | Wu, Mei | en_US |
dc.contributor.author | Wu, Zhi-Fen | en_US |
dc.contributor.author | Chinnaiyan, Arul M. | en_US |
dc.date.accessioned | 2006-09-11T14:27:37Z | |
dc.date.available | 2006-09-11T14:27:37Z | |
dc.date.issued | 2004-03 | en_US |
dc.identifier.citation | Wu, Mei; Wu, Zhi-Fen; Kumar-Sinha, Chandan; Chinnaiyan, Arul; Merajver, Sofia D.; (2004). "RhoC Induces Differential Expression of Genes Involved in Invasion and Metastasis in MCF10A Breast Cells." Breast Cancer Research and Treatment 84(1): 3-12. <http://hdl.handle.net/2027.42/44221> | en_US |
dc.identifier.issn | 0167-6806 | en_US |
dc.identifier.issn | 1573-7217 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/44221 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=14999149&dopt=citation | en_US |
dc.description.abstract | Inflammatory breast cancer (IBC) is the most deadly form of breast cancer in humans presumably due to its ability to metastasize from its inception. In our laboratory, overexpression of RhoC GTPase was observed to be specific for IBC tumors, but not for stage-matched, non-IBC tumors. RhoC is known to contribute to an IBC-like phenotype in HPV-E6E7 immortalized breast cells. To further study the effect of RhoC overexpression on IBC metastasis, we generated stable transfectants of spontaneous immortalized mammary epithelial cells (MCF10A) overexpressing wild-type RhoC or a constitutively active RhoC mutant (G14V). Both the RhoC wild type and the G14V transfectants were highly invasive and proliferated more rapidly compared to vector-only control clones. Overexpression of RhoC led to an increase in actin stress fiber and focal adhesion contact formation. Comparative microarray analysis of these clones further revealed that RhoC overexpression upregulated 108 genes whereas seven genes were down-regulated. We have further verified by quantitative RT-PCR that genes involved in cell proliferation, invasion/adhesion, and angiogenesis were modulated by RhoC. This work suggests strong candidates for the downstream oncogenic functions of RhoC. | en_US |
dc.format.extent | 285963 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Kluwer Academic Publishers; Springer Science+Business Media | en_US |
dc.subject.other | Motility | en_US |
dc.subject.other | Breast Cancer | en_US |
dc.subject.other | Medicine & Public Health | en_US |
dc.subject.other | Oncology | en_US |
dc.subject.other | Invasion | en_US |
dc.subject.other | MCF10A | en_US |
dc.subject.other | Microarray | en_US |
dc.subject.other | RhoC | en_US |
dc.title | RhoC Induces Differential Expression of Genes Involved in Invasion and Metastasis in MCF10A Breast Cells | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Obstetrics and Gynecology | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbsecondlevel | Oncology and Hematology | en_US |
dc.subject.hlbsecondlevel | Otolaryngology | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbsecondlevel | Ophthalmology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, MI, USA; Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, MI, USA; Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI, USA; Unit1, Institute of Bioinformatics, Bangalore, India | en_US |
dc.contributor.affiliationum | Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, MI, USA; Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 14999149 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/44221/1/10549_2004_Article_5264607.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1023/B:BREA.0000018426.76893.21 | en_US |
dc.identifier.source | Breast Cancer Research and Treatment | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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