Activation of KRAS promotes the mesenchymal features of basal-type breast cancer.
- Author:
Rae Kwon KIM
1
;
Yongjoon SUH
;
Ki Chun YOO
;
Yan Hong CUI
;
Hyeonmi KIM
;
Min Jung KIM
;
In Gyu KIM
;
Su Jae LEE
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- MeSH: Animals; Breast Neoplasms/*genetics/metabolism/pathology; Cell Line, Tumor; Cell Transformation, Neoplastic/genetics/metabolism; Disease Models, Animal; Epithelial-Mesenchymal Transition/*genetics; Female; Gene Expression Regulation, Neoplastic; Gene Knockdown Techniques; Heterografts; Humans; Neoplasm Invasiveness; Neoplasm Metastasis; Phenotype; Proto-Oncogene Proteins/*genetics/metabolism; *Transcriptional Activation; ras Proteins/*genetics/metabolism
- From:Experimental & Molecular Medicine 2015;47(1):e137-
- CountryRepublic of Korea
- Language:English
- 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.
