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Updated: Nov 10, 2025

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miR-493 by regulating of c-Jun targets Wnt5a/PD-L1-inducing esophageal cancer cell development

Wei Bian1, Yishuai Li2,3, Haiyong Zhu2

  • 1Department of Hepatobiliary Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

Thoracic Cancer
|April 1, 2021
PubMed
Abstract

Insights

MicroRNA-493 (miR-493) plays a key role in esophageal cancer (EC) by forming a feedback loop with Wnt5A and c-JUN. This loop impacts EC cell growth and invasion, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Esophageal cancer (EC) is a prevalent global malignancy with poor survival rates.
  • MicroRNA (miRNA) dysregulation is a known factor in cancer development, particularly in EC pathogenesis.
  • Understanding miRNA involvement in EC is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the miR-493/Wnt5A/c-JUN signaling pathway in esophageal cancer.
  • To elucidate the mechanistic roles of this pathway in EC cell proliferation, migration, and invasion.

Main Methods:

  • In vivo and in vitro experiments were conducted.
  • Mechanistic roles were explored in EC9706 and TE13 cell lines and EC specimens.
  • Multiple validation steps were employed to confirm findings.

Main Results:

  • Overexpression of miR-493 reduced EC cell proliferation, migration, and invasion.
  • miR-493 downregulation correlated with poorer prognosis and Wnt5A levels in EC.
  • A negative feedback loop was identified where miR-493 inhibits c-JUN and Wnt5A, while c-JUN suppresses miR-493 expression.

Conclusions:

  • The miR-493/Wnt5A/c-JUN loop is a critical molecular feedback mechanism in esophageal cancer development.
  • This pathway represents a potential therapeutic target for esophageal cancer treatment.
Keywords:
PD-L1Wnt5Ac-JUNesophageal cancer prognosismiR-493

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