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

Yun-Xia Xie1, Zhi-Hao Zhou2, Shu-Wen Liu1

  • 1Academy of Medical Science, Zhengzhou University, Zhengzhou 450000, China.

Aging
|May 12, 2023
PubMed

Insights

This study reveals that reduced microRNA-497 (miR-497) levels in esophageal cancer (EC) promote tumor growth and chemotherapy resistance by increasing QKI expression. Restoring miR-497 shows therapeutic potential for EC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Esophageal cancer (EC) is a highly lethal malignancy.
  • MicroRNAs (miRNAs) play roles in cancer development, but miR-497's function in EC is unclear.

Purpose of the Study:

  • To investigate the role and mechanism of miR-497 in esophageal cancer tumorigenesis.
  • To explore miR-497 as a potential biomarker and therapeutic target for EC.

Main Methods:

  • Assessed miR-497 expression in EC tissues and cells.
  • Overexpressed miR-497 in EC cells to evaluate effects on proliferation, migration, and tube formation.
  • Identified QKI as a direct target of miR-497.
  • Investigated miR-497's impact on chemotherapy response and tumor growth in vivo.

Main Results:

  • miR-497 expression was significantly downregulated in EC specimens and cells.
  • Forced miR-497 expression inhibited EC cell proliferation, migration, and tube formation.
  • miR-497 directly targets and suppresses QKI expression.
  • Overexpression of miR-497 enhanced chemotherapy efficacy and reduced tumor growth in vivo.

Conclusions:

  • miR-497 acts as a tumor suppressor in esophageal cancer.
  • Downregulation of miR-497 leads to increased QKI expression and chemoresistance in EC.
  • miR-497 is a potential biomarker for EC progression and a promising therapeutic target.
Keywords:
QKIchemotherapy resistanceesophageal cancermiRNA-497tumor growth

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