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MicroRNA-145 exerts tumor-suppressive and chemo-resistance lowering effects by targeting CD44 in gastric cancer

Jian-Feng Zeng1, Xiao-Qiu Ma1, Lin-Pei Wang1

  • 1Jian-Feng Zeng, Lin-Pei Wang, Wei Wang, Department of General Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.

World Journal of Gastroenterology
|April 22, 2017
PubMed
Abstract

Insights

MicroRNA (miR)-145 targets CD44 in gastric cancer cells, inhibiting tumor growth and enhancing chemo-sensitivity. This miR-145/CD44 interaction is crucial for regulating cancer stem cell properties and treatment response.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Gastric cancer is a leading cause of cancer-related mortality worldwide.
  • Cancer stem cells (CSCs) are implicated in tumor growth, metastasis, and therapeutic resistance.
  • The roles of specific microRNAs and their targets in gastric cancer progression are under active investigation.

Purpose of the Study:

  • To investigate the functional relationship between CD44 and microRNA (miR)-145 in gastric cancer.
  • To elucidate the mechanism by which miR-145 influences CD44 expression and its downstream effects.
  • To assess the impact of the miR-145/CD44 axis on gastric cancer stem cell characteristics and chemosensitivity.

Main Methods:

  • Quantification of CD44 and miR-145 levels in gastric cancer cells.
  • Luciferase reporter assays and Western blotting to confirm direct targeting of CD44 by miR-145.
  • Tumor sphere and MTT assays to evaluate self-renewal and chemo-resistance capabilities.
  • Manipulation of miR-145 and CD44 expression to assess functional consequences.

Main Results:

  • CD44 expression was elevated, while miR-145 levels were reduced in gastric cancer cells enriched for CSCs.
  • miR-145 directly targets the 3'-untranslated region of CD44, repressing its expression.
  • Overexpression of CD44 promoted tumor sphere formation and chemo-resistance, while inhibiting miR-145 enhanced CD44 activity.
  • Restoration of miR-145 inhibited CSC properties and increased chemosensitivity, effects that were abrogated by concurrent CD44 overexpression.

Conclusions:

  • The miR-145/CD44 interaction is a key regulatory mechanism in gastric cancer.
  • Targeting this pathway holds potential for modulating tumor growth and overcoming chemo-resistance.
  • Understanding this molecular axis could inform novel therapeutic strategies for gastric cancer treatment.
Keywords:
CD44Chemo-resistanceGastric cancer stem cellsmiR-145

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