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m1A Regulated Genes Modulate PI3K/AKT/mTOR and ErbB Pathways in Gastrointestinal Cancer

Yueshui Zhao1, Qijie Zhao1, Parham Jabbarzadeh Kaboli1

  • 1Laboratory of Molecular Pharmacology, Department of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou, 646000, Sichuan, PR China; South Sichuan Institution for Translational Medicine, Luzhou, 646000, Sichuan, PR China.

Translational Oncology
|July 29, 2019
PubMed
Abstract

Insights

N1-methyladenosine (m1A) regulators are dysregulated in gastrointestinal cancers, impacting cell proliferation via the ErbB and mTOR pathways. This study reveals m1A

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Gene expression is regulated by protein networks.
  • N1-methyladenosine (m1A) is an RNA modification with an unclear role in cancer.
  • The biogenesis and influence of m1A in tumor development require further investigation.

Purpose of the Study:

  • To investigate the role of m1A regulators in gastrointestinal (GI) cancers.
  • To identify signaling pathways influenced by m1A regulators.
  • To understand the impact of m1A modification on tumor development.

Main Methods:

  • Analysis of TCGA data for five GI cancers.
  • Investigation of m1A-related enzyme features using cBioPortal.
  • Bioinformatic analysis of m1A regulator impact on downstream pathways.
  • RNA-seq analysis following ALKBH3 knockdown.

Main Results:

  • Observed dysregulation and genetic alterations of m1A enzymes in tumors.
  • Identified ErbB and mTOR pathways, with hub genes ErbB2, mTOR, and AKT1S1, as regulated by m1A enzymes.
  • Confirmed decreased expression of ErbB2 and AKT1S1 after ALKBH3 knockdown.
  • Found m1A downstream genes associated with cell proliferation and linked to mTOR.

Conclusions:

  • This study is the first to demonstrate m1A regulator dysregulation in GI cancer.
  • The findings highlight the role of m1A regulators in GI cancer signaling pathways.
  • Contributes to understanding RNA modification's role in cancer.

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