Down-regulation of lncRNA Linc00152 suppressed cell viability, invasion, migration, and epithelial to mesenchymal transition, and reversed chemo-resistance in breast cancer cells.

Abstract

Breast cancer is one of the most common cancer types in women, and long non-coding RNAs (lncRNAs) were found to play important roles in breast cancer progression. The present study examined the effects of Linc00152 on the breast cancer progression and explored the underlying molecular mechanisms. The expression levels of relevant genes in tissues and cells were detected by quantitative Real-time PCR (qRT-PCR) assay. Cell viability, growth, invasion, and migration were measured by CCK-8, colony formation, transwell invasion, and migration assays, respectively. Western blot was used to detect the expression levels of proteins. The results showed that Linc00152 was highly expressed in the breast cancer tissues compared to their adjacent normal tissues, and Linc00152 was also up-regulated in the breast cancer cell lines compared to normal cell lines. Knock-down of Linc00152 by using siRNAs in breast cancer cell lines (MDA-MB-231 and MCF-7) significantly suppressed cell viability, cell growth, cell invasion and migration as measured by the CCK-8, colony formation, transwell invasion, and migration assays. The qRT-PCR and Western blot results showed that knock-down of Linc00152 suppressed epithelial-mesenchymal transition in breast cancer cell lines. In addition, CCK-8 assay showed that knock-down of Linc00152 in MCF-7/ADR cells reversed the chemo-resistance to doxorubicin. Our results suggested the oncogenic role of Linc00152 in the breast cancer progression. Understanding the role of Linc00152 in breast cancer progression may provide a novel therapeutic target for the treatment of breast cancer.