期刊
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
卷 47, 期 8, 页码 1464-1472出版社
WILEY
DOI: 10.1111/1440-1681.13307
关键词
breast cancer; competing endogenous RNA; doxorubicin resistance; XIST; miR-200c-3p; ANLN
资金
- National Natural Science Foundation of China [81572612]
- Research Innovation Program for Graduate Students of Central South University [2018zzts912, 2019zzts786]
- National Key Clinical Specialist Construction Programs of China [2014kll]
The resistance of breast cancer cells to drugs is a major obstacle to effective cancer chemotherapy. Here, we study the function mechanisms of long non-coding RNA XIST in chemoresistance of breast cancer to doxorubicin. We examined the 50% inhibitive concentration of doxorubicin to MDA-MB-231 and MDA-MB-231/ADM cells, showing that the doxorubicin resistance of MDA-MB-231/ADM cells was much higher than MDA-MB-231 cells. The gene or protein expression of XIST and ANLN were also higher in MDA-MB-231/ADM cells than that in MDA-MB-231 cells. Moreover, XIST overexpression promoted cell proliferation and inhibited apoptosis of doxorubicin-treated MDA-MB-231 cells by promoting ANLN expression. XIST silencing inhibited cell proliferation and promoted apoptosis of doxorubicin-treated MDA-MB-231/ADM cells by inhibiting ANLN expression. Luciferase reporter assay showed that XIST functioned as a competing endogenous RNA to repress miR-200c-3p, which controlled its downstream target ANLN. In conclusion, these data reveal that XIST promotes chemoresistance of breast cancer cells to doxorubicin by sponging miR-200c-3p to upregulate ANLN. This work explores the relationship between lncRNA XIST and doxorubicin resistance in breast cancer cells and highlights a novel therapeutic target for the treatment of breast cancer.
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