Abstract
LncRNA HOX transcript antisense RNA (HOTAIR) is involved in lots of cancers. The pro-survival protein Bcl-w is frequently found in cancer development. However, the effect of HOTAIR on Bcl-w in breast cancer is not well documented. In this study, we first evaluated the correlation between HOTAIR level and Bcl-w expression in clinical breast cancer tissues. We observed that the expression levels of Bcl-w were much higher in the breast cancer samples than that in their paired noncancerous tissues. Moreover, the levels of HOTAIR were positively associated with those of Bcl-w in clinical breast cancer samples. As expected, we observed that HOTAIR was able to up-regulate the expression of Bcl-w in breast cancer cells. Mechanistically, we found that miR-206 was capable of inhibiting the expression of Bcl-w by directly binding to the 3′UTR of Bcl-w mRNA. Interestingly, HOTAIR could increase the expression of Bcl-w through sequestering miR-206 at post-transcriptional level. Functionally, our data showed that HOTAIR-induced Bcl-w by miR-206 facilitated the proliferation of breast cancer cells. Thus, we conclude that HOTAIR up-regulates Bcl-w to enhance cell proliferation through sequestering miR-206 in breast cancer. Our finding provides new insights into the mechanism of breast cancer mediated by HOTAIR.
Highlights
In this study, we seek to explore whether lincRNA HOX transcript antisense RNA (HOTAIR) enhances the development of breast cancer through miR-206 targeting Bcl-w
We found that Bcl-w was overexpressed in 28 clinical breast cancer tissues (Fig. 1a, Wilcoxon’s signed-rank test, p < 0.001)
QRT-PCR analysis demonstrated that HOTAIR expression was positively correlated with Bcl-w expression in clinical breast cancer tissues (Pearson’s correlation, R = 0.8451, p < 0.001, Fig. 1b)
Summary
We seek to explore whether lincRNA HOTAIR enhances the development of breast cancer through miR-206 targeting Bcl-w. We find that HOTAIR increases Bcl-w expression via sequestering miR-206 at post-transcription level, leading to the promotion of breast cancer growth. QRT-PCR analysis demonstrated that HOTAIR expression was positively correlated with Bcl-w expression in clinical breast cancer tissues (Pearson’s correlation, R = 0.8451, p < 0.001, Fig. 1b). Luciferase reporter gene assay demonstrated that miR-206 could dose-dependently inhibit the luciferase activities of pGL-Bcl-w-wt in MCF-7 cells but not pGL-Bcl-w-mut (Fig. 3a).
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