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MiR-323-3p Targeting Transmembrane Protein with EGF-Like and 2 Follistatin Domain (TMEFF2) Inhibits Human Lung Cancer

Ji-Min Fan1, Zheng-Rong Zheng2, Yi-Ming Zeng1

  • 1Department of Pulmonary and Critical Care Medicine, Second Affiliated Hospital of Fujian Medical University, Respiratory Medicine Center of Fujian Province, Quanzhou, Fujian, China (mainland).

Medical Science Monitor : International Medical Journal of Experimental and Clinical Research
|February 4, 2020
PubMed

Insights

MicroRNA-323-3p (miR-323-3p) acts as a lung cancer oncogene, promoting non-small-cell lung cancer (NSCLC) progression by suppressing TMEFF2 and inhibiting AKT/ERK pathways. This microRNA represents a potential therapeutic target for NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Non-small-cell lung cancer (NSCLC) has a low survival rate, necessitating elucidation of its tumorigenesis mechanisms.
  • MicroRNA-323-3p (miR-323-3p) is implicated in various cancers, but its role in NSCLC is not fully understood.

Purpose of the Study:

  • To investigate the expression pattern and biological function of miR-323-3p in NSCLC.
  • To explore the molecular mechanism of miR-323-3p in NSCLC development and progression.

Main Methods:

  • Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) for gene expression analysis.
  • Cell proliferation, migration, invasion, and apoptosis assays to assess biological functions.
  • Dual-luciferase reporter and Western blot assays to determine molecular mechanisms.

Main Results:

  • miR-323-3p expression was significantly upregulated in NSCLC cell lines compared to normal cells.
  • miR-323-3p directly suppressed TMEFF2 expression.
  • miR-323-3p indirectly inhibited AKT and ERK pathway activation, promoting NSCLC progression.

Conclusions:

  • miR-323-3p functions as an oncogene in NSCLC.
  • miR-323-3p is a potential therapeutic target for NSCLC treatment.

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