LncRNA XIST promotes chemoresistance of breast cancer cells to doxorubicin by sponging miR-200c-3p to upregulate ANLN.

Abstract:

: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.

authors

Zhang M,Wang F,Xiang Z,Huang T,Zhou WB

doi

10.1111/1440-1681.13307

subject

Has Abstract

pub_date

2020-08-01 00:00:00

pages

1464-1472

issue

8

eissn

0305-1870

issn

1440-1681

journal_volume

47

pub_type

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