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  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Prmt5-mediated Methylation Of Stat3 Is Required For Lung Cancer Stem Cell Maintenance And Tumour Growth

PRMT5-mediated methylation of STAT3 is required for lung cancer stem cell maintenance and tumour growth

Yoshinori Abe1,2, Takumi Sano2, Naoki Otsuka2

  • 1Laboratory of Molecular Analysis, Nippon Medical School, Tokyo, Japan.

Communications Biology
|May 17, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Protein arginine methyltransferase 5 (PRMT5) activates Signal transducer and activator of transcription 3 (STAT3) in lung cancer. This STAT3 activation by PRMT5 drives tumor growth and cancer stem cell maintenance, offering a new therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Signal transducer and activator of transcription 3 (STAT3) is constitutively active in many cancers, promoting proliferation and cancer stem cell (CSC) maintenance.
  • The precise mechanism sustaining STAT3 activation in cancer cells is not fully understood.
  • Tyrosine kinases like JAK and SRC activate STAT3, but downstream regulation remains unclear.

Purpose of the Study:

  • To elucidate the mechanism of STAT3 activation in non-small cell lung cancer (NSCLC).
  • To investigate the role of PRMT5 in STAT3 activation and its impact on tumor progression.
  • To identify PRMT5 as a potential therapeutic target for NSCLC.

Main Methods:

  • Investigated the direct interaction and methylation of STAT3 by PRMT5 in NSCLC cells.

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  • Analyzed the effect of PRMT5-mediated STAT3 methylation on STAT3 tyrosine phosphorylation.
  • Utilized a STAT3 mutant (R609K) to assess the functional significance of arginine 609 methylation in vivo.
  • Examined the positive feedback loop between STAT3 and PRMT5 expression.

    • Main Results:

    • PRMT5 directly methylates STAT3, enhancing its activated tyrosine phosphorylation in NSCLC cells.
    • STAT3 induces PRMT5 expression, establishing a positive feedback loop.
    • Methylation of STAT3 at arginine 609 by PRMT5 is crucial for its transcriptional activity, tumor growth, and CSC maintenance.
    • NSCLC cells with a STAT3 R609K mutation exhibited significantly impaired tumor growth in vivo.

    Conclusions:

    • PRMT5-mediated methylation of STAT3 is a key mechanism sustaining STAT3 activation in NSCLC.
    • The STAT3-PRMT5 feedback loop contributes to tumor progression and CSC maintenance.
    • Targeting PRMT5 offers a promising therapeutic strategy for NSCLC treatment.