miR-34c-3p Inhibits Nasopharyngeal Carcinoma Development via Inhibiting M2 Polarization of Macrophages

Yu Zi Ji1, Yu Jie Wang1, Ji Qing Ma1

  • 1Department of Otolaryngology Head and Neck surgery, Henan Provincial People's Hospital (People's Hospital of Zhengzhou University), Zhengzhou 450003, Henan, China.

Abstract

Insights

MicroRNA 34c-3p (miR-34c-3p) inhibits nasopharyngeal carcinoma (NPC) progression by targeting SLC7A11 and suppressing M2 macrophage polarization. This finding offers a potential new therapeutic strategy for NPC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Nasopharyngeal carcinoma (NPC) is a prevalent head and neck cancer.
  • The role and mechanism of miR-34c-3p in NPC remain largely unexplored.
  • Down-regulation of miR-34c-3p is observed in NPC tissues.

Purpose of the Study:

  • To investigate the biological function of miR-34c-3p in NPC.
  • To elucidate the underlying molecular mechanisms of miR-34c-3p action in NPC.
  • To evaluate miR-34c-3p as a potential therapeutic target for NPC.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were used to assess miR-34c-3p, CD86, and CD206 expression.
  • Cell counting kit-8 (CCK8) and transwell assays were performed to evaluate NPC cell proliferation, migration, and invasion.
  • Flow cytometry, immunohistochemistry, and hematoxylin-eosin (HE) staining were utilized to analyze macrophage polarization and tumor pathology.

Main Results:

  • miR-34c-3p mimic transfection inhibited M2 macrophage polarization by targeting SLC7A11.
  • M2 macrophages transfected with miR-34c-3p mimic suppressed NPC cell proliferation, migration, and invasion.
  • In vivo studies demonstrated that miR-34c-3p mimics inhibited tumor growth and reduced inflammatory infiltration.

Conclusions:

  • miR-34c-3p plays a crucial role in regulating NPC progression.
  • Targeting miR-34c-3p offers a novel therapeutic strategy for NPC.
  • This study provides new insights into NPC pathogenesis and treatment.

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