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Research Paper|Volume 15, Issue 9|pp 3791—3806

microRNA-497 slows esophageal cancer development and reverses chemotherapy resistance through its target QKI

Yun-Xia Xie1, Zhi-Hao Zhou2, Shu-Wen Liu1, Ye Zhang3, Wen-Jing Liu3, Rui-Ke Zhang1, Ming-Liang He4, Jian-Ge Qiu1, Lin Wang1,2, Bing-Hua Jiang1
  • 1Academy of Medical Science, Zhengzhou University, Zhengzhou 450000, China
  • 2BGI College and Henan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450000, China
  • 3The Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, Zhengzhou University, Zhengzhou 450000, China
  • 4Department of Biomedical Sciences, City University of Hong Kong, Hong Kong 999077, Hong Kong
Received: February 2, 2023Accepted: May 1, 2023Published: May 11, 2023
https://doi.org/10.18632/aging.204713

Copyright: © 2023 Xie et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Esophageal cancer (EC) is considered one of the most lethal cancers in human beings, and multiple miRNAs have been investigated to be involved in EC development by targeting their target genes. However, the function and related mechanism of miRNA-497 on EC tumorigenesis remain uncertain. This study first demonstrated that the expression levels of miR-497 in esophageal cancer specimens and cells were down-regulated. Forced expression of miR-497 inhibited cell proliferation, tube formation and migration in EC cells. To further investigate the potential molecular mechanism of miR-497 suppression in regulating EC, we found that miR-497 directly binds to the 3'-untranslational region of QKI, miR-497 overexpression suppressed QKI expression. We further found that overexpression of miR-497 enhanced the effect of chemotherapy in EC cell lines, and prevented the tumor growth of EC in vivo. Our findings indicated that miR-497 suppression increased QKI expression and therapeutic resistance of esophageal cancer, which is likely to be a biomarker of EC progression and potential therapeutic target.