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FOXD3-AS1 suppresses the progression of non-small cell lung cancer by regulating miR-150/SRCIN1axis

Tao Ji1, Yanan Zhang1, Zheng Wang1

  • 1Department of Cardiothoracic Surgery, General Hospital of Central Theater Command, Wuhan, Hubei, China.

Cancer Biomarkers : Section a of Disease Markers
|September 14, 2020
PubMed
Abstract

Insights

Long non-coding RNA FOXD3-AS1 inhibits non-small cell lung cancer (NSCLC) progression by targeting miR-150 and upregulating SRCIN1. This finding offers a potential therapeutic target for NSCLC treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • RNA Biology

Background:

  • Long non-coding RNA (lncRNA) FOXD3-AS1's role in human cancers is known, but its specific function in non-small cell lung cancer (NSCLC) remains unclear.
  • Understanding lncRNA mechanisms is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To investigate the role and mechanism of FOXD3-AS1 in non-small cell lung cancer (NSCLC).
  • To explore the potential of FOXD3-AS1 as a therapeutic target for NSCLC.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) for gene expression analysis.
  • Cell proliferation (CCK-8, BrdU) and invasion (Transwell) assays in NSCLC cell lines.
  • Dual luciferase reporter gene, RNA immunoprecipitation (RIP), and Western blot assays to elucidate molecular interactions.

Main Results:

  • FOXD3-AS1 expression was significantly downregulated in NSCLC tissues and cell lines.
  • Low FOXD3-AS1 expression correlated with advanced tumor grade and lymph node metastasis.
  • FOXD3-AS1 overexpression inhibited NSCLC cell proliferation and invasion, while knockdown promoted these processes.
  • FOXD3-AS1 was confirmed to target and suppress miR-150, leading to the upregulation of SRCIN1.

Conclusions:

  • FOXD3-AS1 acts as a tumor suppressor in NSCLC.
  • FOXD3-AS1 inhibits NSCLC progression by indirectly upregulating SRCIN1 via targeting miR-150.
  • Targeting the FOXD3-AS1/miR-150/SRCIN1 axis may represent a novel therapeutic strategy for NSCLC.
Keywords:
FOXD3-AS1MiR-150NSCLCSRCIN1

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