Abstract
Objective To explore the role and mechanism of keratin 19 (KRT19) in breast cancer. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) assay was used to determine KRT19 levles in 35 cases of breast cancer tissues and normal tissues. The correlation between KRT19 levels and clinical property of breast cancer was analyzed. Meanwhile, the expression levels of KRT19 in several breast cancer cells and mammary epithelial cell Michigan cancer foundation (MCF)-10A were evaluated by qRT-PCR assay. Over-expressed and knocked-down KRT19 in breast cancer cells, 3-(4, 5-dimenthylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay was performed to detect the proliferation and chemosensitivity of these cells. The ability of forming colon of these breast cancer cells with treated KRT19 was studied via colony-forming unit assays. Western blot assay was performed to determine expression levels of cell cycler related proteins. Results KRT19 was upregulated in breast cancer tissues comparing to normal tissues. KRT19 was positively related to tumor node metastasis (TNM) stage and distant metastasis of breast cancer. Similarly, KRT19 was highly expressed in breast cancer cells compared to mammary epithelial cell MCF-10A. The proliferation and colony-forming ability was significantly enhanced in MCF-7 cell with overexpressed KRT19. MTS assay showed that chemosensitivity of MCF-7 cells with overexpression of KRT19 was much more remarkably reduced than the control group. However, knocking down KRT19 in breast cancer cells MDA-MB-231 got the opposite results. Western blot assay suggested that KRT19 could obviously upregulated cyclin-dependent kinase 1 (CDK1) but not p27 expression levels. Conclusions KRT19 was upregulated in breast cancer tissues and was positively related to TNM stage and distant metastasis of breast cancer. KRT19 can significantly enhance proliferation and chemoresistance of breast cancer cells via upregulating CDK1. Key words: Keratin-19; CDC2 protein kinase; Breast neoplasms; Cell proliferation; Drug tolerance
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