Abstract
Due to the accumulating evidence that has demonstrated the vital role of cancer stem cells (CSCs) in tumor initiation, progression and metastasis, the mechanisms that maintain the stemness of CSCs have attracted increasing attention. Metastasis-associated lung adenocarcinoma transcript-1 (MALAT-1), a long non-coding RNA, which has been revealed to be associated with the malignant behavior of tumors, performs a critical role in maintaining the stemness in several CSCs. In the present study, it was hypothesized that MALAT-1 promotes stem cell-like phenotypes in breast cancer cells. The present data demonstrated that the expression of MALAT-1 was higher in the CSC subpopulation compared with that in the overall MCF7 cell group and that the knockdown of MALAT-1 decreased the proportion of CSCs. The self-renewal assay also demonstrated that knockdown of MALAT-1 decreased the sphere formation rate in vitro. In addition, MALAT-1 is also able to regulate the proliferation, colony formation, migration and invasion of CSCs in vitro. The underlying mechanisms may involve the regulation of self-renewal-associated factors, including sex-determining region Y-box 2 (Sox-2). Taken together, the present study demonstrated that MALAT-1 affects the stem cell-like phenotypes in breast cancer cells through regulation of Sox-2.