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Updated: Jun 11, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

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ADAR1-regulated miR-142-3p/RIG-I axis suppresses antitumor immunity in nasopharyngeal carcinoma

Haoyuan Xu1, Wanpeng Li1, Kai Xue1

  • 1Department of Otolaryngology-Head and Neck Surgery, Affiliated Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, 200031, China.

Non-Coding RNA Research
|October 1, 2024
PubMed

Insights

MicroRNAs (miRNAs) like miR-142-3p promote nasopharyngeal carcinoma (NPC) progression by suppressing immune responses. Targeting miR-142-3p and its processing by ADAR1 offers a new therapeutic strategy for NPC patients with recurrent tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Tumor progression in nasopharyngeal carcinoma (NPC) significantly impacts patient prognosis.
  • MicroRNAs (miRNAs) play a role in tumor immunity, but their specific functions in NPC are not fully understood.

Purpose of the Study:

  • To identify key miRNAs involved in NPC progression and immune evasion.
  • To elucidate the molecular mechanisms by which identified miRNAs regulate NPC growth and antitumor immunity.

Main Methods:

  • Comprehensive miRNA sequencing and tissue microarray analysis to identify prognostic miRNAs in recurrent NPC.
  • RNA sequencing, cellular, and tissue assays to determine downstream targets and signaling pathways of miR-142-3p.
  • In vitro and in vivo functional assays to assess the impact of target gene overexpression.
  • Analysis of protein-protein interactions and miRNA processing pathways.

Main Results:

  • miR-142-3p was significantly upregulated in recurrent NPC and associated with poor prognosis.
  • CFL2 and WASL were identified as direct downstream targets of miR-142-3p, and their overexpression reversed malignant phenotypes.
  • miR-142-3p was found to inhibit the RIG-I immune defense pathway by preventing IRF3, IRF7, and p65 nuclear translocation.
  • ADAR1 was shown to interact with Dicer, promoting mature miR-142-3p formation.

Conclusions:

  • ADAR1-mediated miR-142-3p processing promotes NPC tumor progression and suppresses antitumor immunity.
  • miR-142-3p represents a potential prognostic biomarker for recurrent NPC.
  • Targeting miR-142-3p and its processing pathway presents a promising therapeutic strategy for NPC.
Keywords:
Nasopharyngeal carcinomaRIG-ITumor immune responsemiR-142-3p

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