Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 Expression

被引:10
作者
Li, Lei [1 ]
Lv, Guohua [1 ]
Wang, Bing [1 ]
Ma, Hong [1 ]
机构
[1] Cent South Univ, Xiangya Hosp 2, Dept Spine Surg, Changsha 410011, Hunan, Peoples R China
关键词
KCNQ1OT1; MDR; miR-27b-3p; ATF2; chordoma; KNOCKDOWN; PROLIFERATION; PROGRESSION; METASTASIS; CANCER;
D O I
10.2147/CMAR.S250611
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: Chordoma, a rare bone tumor, occurs most commonly at the sacrococcygeal and skull base region. To date, chemotherapy is used to treat patients with advanced-stage chordoma. However, multidrug resistance (MDR) greatly hinders the effect of chemotherapy in chordoma. Here, we studied the correlation between KCNQ1OT1 and chemotherapy resistance. Methods: RT-PCR assay was used to examine KCNQ1OT1, miR-27b-3p, and ATF2 mRNA expression. CCK8 assay was exercised to detect IC 50 values of cisplatin in chordoma cells. ATF2 protein expression was detected by Western blot. Results: KCNQ1OT1 was increased in chemotherapy-resistant patients and cisplatinresistant cells, and downregulation of KCNQ1OT1 expression weakened MDR in chordoma. In addition, KCNQ1OT1 promoted MDR in chordoma by sponging miR-27b-3p and subsequently increasing ATF2 expression. Conclusion: KCNQ1OT1 is proved to be strikingly raised in the chemotherapy-resistant group and to promote MDR in chordoma. Our findings demonstrated the role of the KCNQ1OT1/miR-27b-3p/ATF2 axis in MDR of chordoma, which provides new insight into the molecular mechanism of chordoma MDR, and may determine the effect of therapy after receiving chemotherapy by detecting the expression of KCNQ1OT1 in serum.
引用
收藏
页码:7847 / 7853
页数:7
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