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DNMT1 Mediated CAHM Repression Promotes Glioma Invasion via SPAK/JNK Pathway

Yadi Xu1, Zelin Li2,3, Tian Huai2,3

  • 1Ultrasonography Department, Hubei Hospital of Traditional Chinese Medicine, Wuhan, China.

Cellular and Molecular Neurobiology
|July 6, 2021
PubMed

Insights

Colorectal adenocarcinoma hypermethylated (CAHM) long non-coding RNA acts as a tumor suppressor in gliomas. Its reduced expression, linked to poor survival, inhibits glioma cell proliferation and invasion, suggesting therapeutic potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Gliomas are aggressive brain tumors with poor prognosis.
  • Aberrant DNA methylation is a key mechanism in tumor suppressor gene inactivation.
  • The role of long non-coding RNA colorectal adenocarcinoma hypermethylated (CAHM) in gliomas is currently unknown.

Purpose of the Study:

  • To investigate the expression, regulation, and function of CAHM in glioma.
  • To determine the prognostic value of CAHM in glioma patients.

Main Methods:

  • Analysis of 969 glioma samples from public databases (CGGA and Gravendeel).
  • Assessment of CAHM expression correlation with clinical and molecular features.
  • Investigation of CAHM regulation by DNA methyltransferase 1 (DNMT1) and its reversal by 5-Aza-2'-deoxycytidine (5-Aza).
  • Functional studies including cell proliferation, clone formation, invasion, and migration assays.
  • Gene Ontology (GO) analysis and pathway analysis (SPAK/MAPK).

Main Results:

  • CAHM expression inversely correlated with glioma grade, molecular subtype, IDH mutation, and 1q/19p codel status.
  • CAHM hypermethylation by DNMT1 was observed, and its expression was restored by 5-Aza.
  • Lower CAHM expression was associated with reduced overall survival in both primary and recurrent gliomas.
  • CAHM functions in regulating cell development, nervous system development, neurogenesis, and integrin-mediated signaling.
  • CAHM overexpression inhibited glioma cell proliferation, clone formation, invasion, and migration, partly via the SPAK/MAPK pathway.

Conclusions:

  • CAHM acts as a tumor suppressor in gliomas.
  • CAHM expression is epigenetically regulated and has prognostic significance.
  • CAHM may represent a potential therapeutic target for glioma treatment.
Keywords:
CAHMDNA methylationGlioma invasionLncRNASPAK/MAPK pathway

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