Mitogen activated protein kinase pathway is involved in RhoC GTPase induced motility, invasion and angiogenesis in inflammatory breast cancer
dc.contributor.author | van Golen, Kenneth L. | en_US |
dc.contributor.author | Wei Bao, Li | en_US |
dc.contributor.author | Pan, Quintin | en_US |
dc.contributor.author | Miller, Fred R. | en_US |
dc.contributor.author | Fen Wu, Zhi | en_US |
dc.contributor.author | Merajver, Sofia D. | en_US |
dc.date.accessioned | 2006-09-08T20:29:57Z | |
dc.date.available | 2006-09-08T20:29:57Z | |
dc.date.issued | 2002-05 | en_US |
dc.identifier.citation | van Golen, Kenneth L.; Wei Bao, Li; Pan, Quintin; Miller, Fred R.; Fen Wu, Zhi; Merajver, Sofia D.; (2002). "Mitogen activated protein kinase pathway is involved in RhoC GTPase induced motility, invasion and angiogenesis in inflammatory breast cancer." Clinical & Experimental Metastasis 19(4): 301-311. <http://hdl.handle.net/2027.42/42584> | en_US |
dc.identifier.issn | 0262-0898 | en_US |
dc.identifier.issn | 1573-7276 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/42584 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12090470&dopt=citation | en_US |
dc.description.abstract | Inflammatory breast cancer (IBC) is the most lethal form of locally advanced breast cancer known. IBC carries a guarded prognosis primarily due to rapid onset of disease, typically within six months, and the propensity of tumor emboli to invade the dermal lymphatics and spread systemically. Although the clinical manifestations of IBC have been well documented, until recently little was known about the genetic mechanisms underlying the disease. In a comprehensive study aimed at identifying the molecular mechanisms responsible for the unique IBC phenotype, our laboratory identified overexpression of RhoC GTPase in over 90% of IBC tumors in contrast to 36% of stage-matched non-IBC tumors. We also demonstrated that overexpression of RhoC GTPase in human mammary epithelial (HME) cells nearly recapitulated the IBC phenotype with regards to invasion, motility and angiogenesis. In the current study we sought to delineate which signaling pathways were responsible for each aspect of the IBC phenotype. Using well-established inhibitors to the mitogen activated protein kinase (MAPK) and phosphatidylinositol-3 kinase (PI3K) pathways. We found that activation of the MAPK pathway was responsible for motility, invasion and production of angiogenic factors. In contrast, growth under anchorage independent conditions was dependent on the PI3K pathway. | en_US |
dc.format.extent | 247176 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 | Medicine & Public Health | en_US |
dc.subject.other | Cancer Research | en_US |
dc.subject.other | Oncology | en_US |
dc.subject.other | Hematology | en_US |
dc.subject.other | Surgical Oncology | en_US |
dc.subject.other | Angiogenic Factors | en_US |
dc.subject.other | C3 Exotransferase | en_US |
dc.subject.other | Human Mammary Epithelial (HME) Cells | en_US |
dc.subject.other | Inflammatory Breast Cancer (IBC) | en_US |
dc.subject.other | Inhibitors | en_US |
dc.subject.other | Invasion | en_US |
dc.subject.other | Mitogen Activated Protein Kinase (MAPK) | en_US |
dc.subject.other | Motility | en_US |
dc.subject.other | Phosphatidylinositol-3 Kinase (PI3K) | en_US |
dc.subject.other | RhoC GTPase | en_US |
dc.title | Mitogen activated protein kinase pathway is involved in RhoC GTPase induced motility, invasion and angiogenesis in inflammatory breast cancer | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Oncology and Hematology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, , University of Michigan Comprehensive Cancer Center, , , Ann Arbor, , Michigan, , USA, | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, , University of Michigan Comprehensive Cancer Center, , , Ann Arbor, , Michigan, , USA, | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, , University of Michigan Comprehensive Cancer Center, , , Ann Arbor, , Michigan, , USA, | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, , University of Michigan Comprehensive Cancer Center, , , Ann Arbor, , Michigan, , USA, | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, , University of Michigan Comprehensive Cancer Center, , , Ann Arbor, , Michigan, , USA, | en_US |
dc.contributor.affiliationother | Breast Cancer Program, , Barbara Ann Karmanos Cancer Institute, , , Detroit, , Michigan, , USA, | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 12090470 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/42584/1/10585_2004_Article_397672.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1023/A:1015518114931 | en_US |
dc.identifier.source | Clinical & Experimental Metastasis | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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