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The HDAC2-MTA3 interaction induces nonsmall cell lung cancer cell migration and invasion by targeting c-Myc and

Bin Wang1, Xiao-Yong Shen1, Lin-Yue Pan2

  • 1Shanghai Key Laboratory of Clinical Geriatric Medicine, Department of Thoracic Surgery, The Affiliated Huadong Hospital of Fudan University, Shanghai, China.

Molecular Carcinogenesis
|July 4, 2023
PubMed

Insights

This study identifies the histone deacetylase 2 (HDAC2) rs13213007 single-nucleotide polymorphism (SNP) as a risk factor for nonsmall cell lung cancer (NSCLC). Upregulated HDAC2 promotes NSCLC progression by enhancing cell proliferation, migration, and invasion.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Genome-wide association studies have linked numerous single-nucleotide polymorphisms (SNPs) to lung cancer.
  • The specific roles of histone deacetylase 2 (HDAC2) and its SNP rs13213007 in nonsmall cell lung cancer (NSCLC) require further elucidation.

Purpose of the Study:

  • To investigate the functional significance of the HDAC2 rs13213007 SNP in NSCLC.
  • To determine the association between HDAC2 expression, its rs13213007 genotype, and NSCLC progression.
  • To explore the molecular mechanisms by which HDAC2 influences NSCLC cell behavior.

Main Methods:

  • Genotyping and analysis of HDAC2 rs13213007 in NSCLC patients.
  • Immunohistochemical staining to assess HDAC2 expression in tumor tissues.
  • CRISPR/Cas9 gene editing to create cells with specific genotypes.
  • Chromatin immunoprecipitation sequencing (ChIP-seq) and motif analysis.
  • Cell proliferation, migration, and invasion assays (Cell Counting Kit-8, colony formation, wound-healing, Transwell).
  • Co-immunoprecipitation, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and Western blot analysis.

Main Results:

  • HDAC2 rs13213007 was identified as a risk SNP for NSCLC.
  • HDAC2 was upregulated in peripheral blood mononuclear cells (PBMCs) and NSCLC tissues with the rs13213007 A/A genotype.
  • HDAC2 expression correlated with N classification and NSCLC progression.
  • HDAC2 binds to c-Myc in rs13213007 A/A cells, upregulating c-Myc and cyclin D1.
  • HDAC2 promotes NSCLC cell proliferation, migration, and invasion.
  • MTA3 interacts with HDAC2, reducing its expression and rescuing cell migration and invasion.

Conclusions:

  • HDAC2 rs13213007 is a risk SNP associated with NSCLC progression.
  • Upregulated HDAC2, particularly with the A/A genotype, drives NSCLC cell proliferation, migration, and invasion via c-Myc and cyclin D1.
  • MTA3 acts as a negative regulator of HDAC2 in NSCLC.
  • HDAC2 represents a potential therapeutic biomarker for NSCLC.
Keywords:
MTA3histone deacetylase 2migration and invasionnonsmall cell lung cancersingle-nucleotide polymorphism

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