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A Pan-Cancer Analysis of SMARCA4 Alterations in Human Cancers

Ling Peng1, Jisheng Li2, Jie Wu3

  • 1Department of Respiratory Disease, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, China.

Frontiers in Immunology
|October 22, 2021
PubMed
Abstract

Insights

SMARCA4, a key component of the SWI/SNF complex, is highly expressed in many cancers and linked to poorer survival and altered tumor immunity. Its dysregulation impacts cancer progression and immune cell infiltration.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genomics

Background:

  • SMARCA4 is an essential ATPase subunit of the SWI/SNF chromatin remodeling complex.
  • This complex regulates gene transcription by altering chromatin structure.
  • SMARCA4 is increasingly recognized for its significant roles in human cancers.

Purpose of the Study:

  • To explore the potential role of SMARCA4 in various cancer types.
  • To provide insights into the pathologic mechanisms involving SMARCA4 in cancer.
  • To analyze the relationship between SMARCA4 and tumor immunity.

Main Methods:

  • Utilized The Cancer Genome Atlas (TCGA), GTEx, TIMER, and GSEA datasets.
  • Analyzed SMARCA4 expression, mutation, and phosphorylation status.
  • Investigated correlations with survival, pathological stage, DNA methylation, TMB, MSI, MMR, TME, and immune cell infiltration.

Main Results:

  • High SMARCA4 expression observed in most cancers, correlating with poor overall survival.
  • Altered SMARCA4 in lung adenocarcinoma indicated a poorer prognosis.
  • SMARCA4 dysregulation correlated with TMB, MSI, MMR, and DNA methylation, and showed associations with tumor immunity and immune cell infiltration, including negative association with CD8+ T-cell infiltration.

Conclusions:

  • Provided a comprehensive understanding of SMARCA4's oncogenic roles across diverse tumors.
  • Demonstrated a potential correlation between SMARCA4 and tumor immunity.
  • Suggested the involvement of SWI/SNF and ATPase complexes in SMARCA4's functional mechanisms, requiring further validation.
Keywords:
EMTSMARCA4bioinformaticscancerimmunityoncogene

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