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Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of

Lei Li1, Guohua Lv1, Bing Wang1

  • 1Department of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, People's Republic of China.

Cancer Management and Research
|September 14, 2020
PubMed
Abstract

Insights

This study reveals KCNQ1OT1 promotes chemotherapy resistance in chordoma by regulating the miR-27b-3p/ATF2 pathway. Lowering KCNQ1OT1 expression can overcome multidrug resistance (MDR) in chordoma.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Chordoma is a rare bone tumor often treated with chemotherapy.
  • Multidrug resistance (MDR) significantly limits chemotherapy efficacy in advanced chordoma.

Purpose of the Study:

  • To investigate the role of KCNQ1OT1 in chordoma chemotherapy resistance.
  • To elucidate the molecular mechanism underlying KCNQ1OT1-mediated MDR in chordoma.

Main Methods:

  • Quantitative RT-PCR to assess KCNQ1OT1, miR-27b-3p, and ATF2 mRNA levels.
  • CCK8 and Western blot assays to evaluate chemoresistance and protein expression.

Main Results:

  • KCNQ1OT1 expression was elevated in chemotherapy-resistant chordoma patients and cells.
  • Downregulating KCNQ1OT1 reduced MDR in chordoma.
  • KCNQ1OT1 enhances MDR by sponging miR-27b-3p, leading to increased ATF2 expression.

Conclusions:

  • KCNQ1OT1 is a key driver of MDR in chordoma.
  • The KCNQ1OT1/miR-27b-3p/ATF2 axis represents a novel therapeutic target for overcoming chordoma MDR.
  • Serum KCNQ1OT1 levels may predict chemotherapy response in chordoma patients.
Keywords:
ATF2KCNQ1OT1MDRchordomamiR-27b-3p

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