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Updated: Nov 9, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
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PRMT5 Promotes EMT Through Regulating Akt Activity in Human Lung Cancer

Jianhao Huang1,2, Yonghua Zheng3, Xiao Zheng3

  • 1Department of Pulmonary and Critical Care Medicine, Shanghai East Clinical Medical College, 66324Nanjing Medical University, Nanjing, PR China.

Cell Transplantation
|April 8, 2021
PubMed

Insights

Protein arginine methyltransferase 5 (PRMT5) promotes epithelial-mesenchymal transition (EMT) in human lung cancer. Targeting PRMT5 may offer a new therapeutic strategy for lung cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Protein arginine methyltransferase 5 (PRMT5) is implicated in human cancer progression.
  • The role of PRMT5 in epithelial-mesenchymal transition (EMT) in lung cancer remains largely unexplored.
  • Molecular mechanisms underlying PRMT5's function in lung cancer EMT are unknown.

Purpose of the Study:

  • To investigate the biological functions and molecular mechanisms of PRMT5 in human lung cancer EMT.
  • To determine if PRMT5 regulates EMT through specific signaling pathways.
  • To evaluate PRMT5 as a potential therapeutic target for lung cancer.

Main Methods:

  • Analysis of PRMT5 expression in human lung cancer tissues and cell lines.
  • Silencing PRMT5 using lentivirus-mediated shRNA in vivo.
  • Inhibition of PRMT5 using the specific inhibitor GSK591.
  • Assessment of EMT markers and EGFR/Akt signaling pathway activation.

Main Results:

  • PRMT5 is ectopically expressed in human lung cancer.
  • PRMT5 silencing or inhibition reduced EMT markers in a xenograft mouse model.
  • Down-regulation of PRMT5 impaired EGFR/Akt signaling cascades.
  • Re-expression of PRMT5 restored these signaling changes.

Conclusions:

  • PRMT5 acts as a crucial oncogenic regulator promoting EMT in human lung cancer cells.
  • PRMT5 likely regulates EMT via the EGFR/Akt signaling axis.
  • PRMT5 represents a potential therapeutic candidate for human lung cancer treatment.
Keywords:
AktmEGFREMTGSK3βPRMT5lung cancer

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