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, researchers from Jilin University first evaluated the correlation between HOTAIR level and Bcl-w expression in clinical breast cancer tissues. They 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 they expected, the researchers observed that HOTAIR was able to up-regulate the expression of Bcl-w in breast cancer cells. Mechanistically, they 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.
MiR-206/Bcl-w signal mediates HOTAIR-accelerating cell proliferation in breast cancer
(a–c) Proliferation was tested by MTT and BrdU incorporation assays in MCF-7 or T47D cells treated with the indicated plasmids or siRNAs. (d) Colony formation of MCF-7 cells was counted post-transfection with the indicated plasmids or siRNAs.
Functionally, these data showed that HOTAIR-induced Bcl-w by miR-206 facilitated the proliferation of breast cancer cells. Thus, the researchers concluded that HOTAIR up-regulates Bcl-w to enhance cell proliferation through sequestering miR-206 in breast cancer. These finding provides new insights into the mechanism of breast cancer mediated by HOTAIR.