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JWA deficiency induces malignant transformation of murine embryonic fibroblast cells

Hong Qi1, Aiping Li1

  • 1Department of Molecular Cell Biology and Toxicology, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, P.R. China.

Experimental and Therapeutic Medicine
|March 17, 2018
PubMed

Insights

JWA knockout promotes malignant transformation by increasing cell proliferation, migration, and invasion. This suggests JWA acts as an anti-oncogene, potentially inhibiting tumor formation.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • The role of JWA (Jumonji domain containing 1A) in cellular transformation and tumorigenesis is not fully understood.
  • Investigating JWA's function is crucial for understanding cancer development and identifying potential therapeutic targets.

Purpose of the Study:

  • To investigate the effects of JWA knockout on the malignant transformation of murine embryonic fibroblast (MEF) cells.
  • To determine JWA's role in cell proliferation, migration, invasion, colony formation, and epithelial-mesenchymal transition (EMT).
  • To assess the impact of JWA deficiency on tumor formation in vivo.

Main Methods:

  • Generation of a conditional JWA knockout (JWA-/-) mouse model and isolation of MEF cells.
  • Cytological examination to assess proliferation, migration, invasion, and colony formation.
  • Western blot analysis to evaluate EMT-related protein expression (PARP-1, vimentin, β-catenin, E-cadherin).
  • Nude mouse xenograft model to evaluate tumorigenicity.

Main Results:

  • JWA knockout significantly increased MEF cell proliferation, migration, invasion, and colony formation.
  • JWA deficiency led to upregulation of PARP-1, vimentin, and β-catenin, and downregulation of E-cadherin.
  • Subcutaneous inoculation of JWA-/- MEF cells induced tumor formation in mice, unlike wild-type MEF cells.

Conclusions:

  • JWA knockout promotes malignant transformation of MEF cells by enhancing key cellular processes and altering EMT markers.
  • JWA deficiency increases tumorigenicity, indicating that JWA may function as an anti-oncogene.
  • These findings highlight JWA's critical role in suppressing tumor development.
Keywords:
JWAcarcinogenicitycell proliferationepithelial-mesenchymal transitiongene knockoutmalignant transformation

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