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Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
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Comprehensive molecular profiling of the B7 family in gastrointestinal cancer

Qijie Zhao1, Fuyan Hu2, Zhangang Xiao1

  • 1Laboratory of Molecular Pharmacology, Department of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou, Sichuan, China.

Cell Proliferation
|July 13, 2018
PubMed
Abstract

Insights

Deregulation of B7 family molecules is implicated in gastrointestinal (GI) cancer. Specific B7 members like B7-H1, B7-H5, and B7-H6 correlate with poor survival in GI cancers, indicating their role in tumorigenesis.

Area of Science:

  • Immunology
  • Oncology
  • Genetics

Background:

  • The B7 family comprises co-stimulatory/co-inhibitory molecules crucial for T-cell responses.
  • These molecules play a significant role in tumor mortality and malignancy.

Purpose of the Study:

  • To investigate the expression patterns of B7 family members in gastrointestinal (GI) cancers.
  • To explore the upstream regulatory mechanisms, downstream targets, and clinical associations of B7 family members in GI cancers.

Main Methods:

  • Analysis of B7 member expression using FIREHOUSE.
  • Utilized cBioportal for gene mutation, DNA methylation, and clinical parameter association studies.
  • Employed COSMIC for mutation frequency analysis, MEGA7 for phylogenetic trees, and Pfam 31.0 for protein domain analysis.

Main Results:

  • Differential expression of B7 family molecules observed across various GI cancers.
  • High-frequency gene alterations and a negative correlation between promoter methylation and mRNA expression suggest epigenetic deregulation.
  • Overexpression of B7-H1 (pancreatic), B7-H5 (esophageal), and B7-H6 (liver) cancers associated with worse survival.

Conclusions:

  • B7 member deregulation is significantly involved in the tumorigenesis of GI cancers.
  • Identified potential interacting proteins for B7-1/2 and B7-H1/DC through network analysis.

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