Activation of KRAS promotes the mesenchymal features of basal-type breast cancer
Basal-type breast cancers are among the most aggressive and deadly breast cancer subtypes, displaying a high metastatic ability associated with mesenchymal features. However, the molecular mechanisms underlying the maintenance of mesenchymal phenotypes of basal-type breast cancer cells remain obscur...
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| Published in | Experimental & molecular medicine Vol. 47; no. 1; p. e137 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Springer Nature B.V
01.01.2015
Nature Publishing Group |
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| Abstract | Basal-type breast cancers are among the most aggressive and deadly breast cancer subtypes, displaying a high metastatic ability associated with mesenchymal features. However, the molecular mechanisms underlying the maintenance of mesenchymal phenotypes of basal-type breast cancer cells remain obscure. Here, we report that KRAS is a critical regulator for the maintenance of mesenchymal features in basal-type breast cancer cells. KRAS is preferentially activated in basal-type breast cancer cells as compared with luminal type. By loss and gain of KRAS, we found that KRAS is necessary and sufficient for the maintenance of mesenchymal phenotypes and metastatic ability through SLUG expression. Taken together, this study demonstrates that KRAS is a critical regulator for the metastatic behavior associated with mesenchymal features of breast cancer cells, implicating a novel therapeutic target for basal-type breast cancer. |
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| AbstractList | Basal-type breast cancers are among the most aggressive and deadly breast cancer subtypes, displaying a high metastatic ability associated with mesenchymal features. However, the molecular mechanisms underlying the maintenance of mesenchymal phenotypes of basal-type breast cancer cells remain obscure. Here, we report that KRAS is a critical regulator for the maintenance of mesenchymal features in basal-type breast cancer cells. KRAS is preferentially activated in basal-type breast cancer cells as compared with luminal type. By loss and gain of KRAS, we found that KRAS is necessary and sufficient for the maintenance of mesenchymal phenotypes and metastatic ability through SLUG expression. Taken together, this study demonstrates that KRAS is a critical regulator for the metastatic behavior associated with mesenchymal features of breast cancer cells, implicating a novel therapeutic target for basal-type breast cancer.Experimental & Molecular Medicine (2015) 47, e137; doi:10.1038/emm.2014.99; published online 30 January 2015 Basal-type breast cancers are among the most aggressive and deadly breast cancer subtypes, displaying a high metastatic ability associated with mesenchymal features. However, the molecular mechanisms underlying the maintenance of mesenchymal phenotypes of basal-type breast cancer cells remain obscure. Here, we report that KRAS is a critical regulator for the maintenance of mesenchymal features in basal-type breast cancer cells. KRAS is preferentially activated in basal-type breast cancer cells as compared with luminal type. By loss and gain of KRAS, we found that KRAS is necessary and sufficient for the maintenance of mesenchymal phenotypes and metastatic ability through SLUG expression. Taken together, this study demonstrates that KRAS is a critical regulator for the metastatic behavior associated with mesenchymal features of breast cancer cells, implicating a novel therapeutic target for basal-type breast cancer. |
| Author | Lee, Su-Jae Kim, Rae-Kwon Yoo, Ki-Chun Kim, Hyeonmi Kim, Min-Jung Suh, Yongjoon Cui, Yan-Hong Gyu Kim, In |
| Author_xml | – sequence: 1 givenname: Rae-Kwon surname: Kim fullname: Kim, Rae-Kwon organization: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea – sequence: 2 givenname: Yongjoon surname: Suh fullname: Suh, Yongjoon organization: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea – sequence: 3 givenname: Ki-Chun surname: Yoo fullname: Yoo, Ki-Chun organization: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea – sequence: 4 givenname: Yan-Hong surname: Cui fullname: Cui, Yan-Hong organization: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea – sequence: 5 givenname: Hyeonmi surname: Kim fullname: Kim, Hyeonmi organization: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea – sequence: 6 givenname: Min-Jung surname: Kim fullname: Kim, Min-Jung organization: Laboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological and Medical Sciences, Seoul, Korea – sequence: 7 givenname: In surname: Gyu Kim fullname: Gyu Kim, In organization: Department of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute, Daejeon, Korea – sequence: 8 givenname: Su-Jae surname: Lee fullname: Lee, Su-Jae organization: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25633745$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Line, Tumor Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Disease Models, Animal Epithelial-Mesenchymal Transition - genetics Female Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Heterografts Humans Neoplasm Invasiveness Neoplasm Metastasis Original Phenotype Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins p21(ras) ras Proteins - genetics ras Proteins - metabolism Transcriptional Activation |
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| Title | Activation of KRAS promotes the mesenchymal features of basal-type breast cancer |
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