UCA1 confers paclitaxel resistance to ovarian cancer through miR-129/ABCB1 axis

被引：86

作者：

Wang, Junrong ^{[1
]}

Ye, Cong ^{[1
]}

Liu, Junbao ^{[1
]}

Hu, Yubo ^{[1
]}

机构：

[1] Jilin Univ, China Japan Union Hosp, Dept Obstet & Gynecol, Changchun 130033, Jilin, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2018年 / 501卷 / 04期

关键词：

UCA1; miR-129; ABCB1; Paclitaxel resistance; Ovarian cancer; LONG NONCODING RNA; BREAST-CANCER; TRASTUZUMAB RESISTANCE; MULTIDRUG-RESISTANCE; CELLS; PROLIFERATION; CARCINOMA; CHEMORESISTANCE; CHEMOTHERAPY; EXPRESSION;

D O I：

10.1016/j.bbrc.2018.05.104

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Increasing evidence has demonstrated the involvement of dysregulated long non-coding RNAs (lncRNAs) in chemoresistance acting as potential oncogenes or tumor suppressors in various cancers. Nevertheless, the profound molecular mechanisms of lncRNAs in ovarian cancer (OC) chemoresistance is not well elucidated. The objective of this work was to investigate the role and molecular mechanisms of urothelial carcinoma associated 1 (UCA1) in paclitaxel (PTX) resistance in OC. Our results indicated that UCA1 was significantly up-regulated in PTX-resistant OC cells (SKOV3/PTX and HeyA-8/PTX) compared with their parental cells (SKOV3 and HeyA-8). Functionally, UCA1 knockdown sensitized SKOV3/PTX and HeyA-8/PTX cells to PTX through enhancing PTX-induced apoptosis. Mechanistically, UCA1 silencing induced PTX sensitivity of SKOV3/PTX and HeyA-8/PTX cells by de-repressing ABCB1 through sponging miR-129. Collectively, our study elaborated a novel UCA1/miR-129/ABCB1 regulatory axis underlying PTX resistance of OC cells, providing a potential therapeutic target for OC. (C) 2018 Elsevier Inc. All rights reserved.

引用

页码：1034 / 1040

页数：7

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