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Induction and Analysis of Epithelial to Mesenchymal Transition
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Loss of DIP2C in RKO cells stimulates changes in DNA methylation and epithelial-mesenchymal transition

Chatarina Larsson1, Muhammad Akhtar Ali1,2, Tatjana Pandzic1

  • 1Department of Immunology, Genetics and Pathology, Uppsala University, Rudbeck Laboratory, Dag Hammarskjölds väg 20, SE-751 85, Uppsala, Sweden.

BMC Cancer
|July 19, 2017
PubMed
Abstract

Insights

Loss of the disco-interacting protein 2 homolog C (DIP2C) gene in cancer cells causes significant DNA methylation and gene expression changes. This leads to cellular senescence and epithelial-mesenchymal transition, impacting tumor development.

Area of Science:

  • Genetics
  • Cancer Biology
  • Epigenetics

Background:

  • The disco-interacting protein 2 homolog C (DIP2C) gene is implicated in a subset of breast and lung cancers.
  • Its precise role in tumor development remains uncharacterized.

Purpose of the Study:

  • To investigate the function of DIP2C in human cancer cells.
  • To understand the molecular mechanisms underlying DIP2C's role in tumorigenesis.

Main Methods:

  • Engineered DIP2C knockout human cancer cells using genome editing.
  • Performed transcriptome and DNA methylation analyses.
  • Studied effects on cell growth, death pathways, and epithelial-mesenchymal transition (EMT).

Main Results:

  • DIP2C knockout led to cell enlargement, growth retardation, and increased wound closing capacity.
  • Expression profiling identified 780 differentially expressed genes, including CDKN2A, ZEB1, CD44, and CD24.
  • Over 30,000 differentially methylated DNA sites were observed, predominantly hypomethylated, correlating with gene expression changes, particularly in EMT and cell death pathways.
  • Increased cellular senescence markers were detected in DIP2C knockout cells.

Conclusions:

  • Loss of DIP2C significantly alters DNA methylation and gene expression in cancer cells.
  • DIP2C inactivation promotes cellular senescence and epithelial-mesenchymal transition (EMT).
  • These findings highlight DIP2C's role in cancer development and progression.
Keywords:
CancerDIP2CDNA methylationEpithelial-mesenchymal transition (EMT)Gene knockoutTumour cell biologyrAAV-mediated gene targeting

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