PVT1-derived miR-1207-5p promotes breast cancer cell growth by targeting STAT6

Abstract

Accumulating evidences indicate ectopic expression of noncoding RNAs are responsible for breast cancer progression. Increased non-coding RNA PVT1, the host gene of microRNA-1207-5p (miR-1207-5p), has been associated with breast cancer proliferation. However, how PVT1 functions in breast cancer is still not clear. In this study, we show a PVT1 derived microRNA, miR-1207-5p, which promotes the proliferation of breast cancer cells by directly regulating STAT6. We first confirm the positive correlated expression pattern between PVT1 and miR-1207-5p by observing consistent induced expression by estrogen, and overexpression in breast cancer cell lines and breast cancer patient specimens. Moreover, silence of PVT1 also decreased miR-1207-5p expression. Furthermore, increased miR-1207-5p expression promoted, while decreased miR-1207-5p expression suppressed cell proliferation, colony formation and cell cycle progression in breast cancer cell lines. Mechanistically, a novel target of miR-1207-5p, STAT6, was identified by a luciferase reporter assay. miR-1207-5p overexpression decreased the levels of STAT6, which activated CDKN1A and CDKN1B to regulate cell cycle. We also confirmed reversely correlated expression level of miR-1207-5p and STAT6 in breast cancer samples. Therefore, our findings demonstrate that PVT1-derived miR-1207-5p promotes the proliferation of breast cancer cells by targeting STAT6, which in turn controls CDKN1A and CDKN1B expression. These findings suggest miR-1207-5p might be a potential target for breast cancer therapy.

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