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BTG2 suppresses renal cell carcinoma progression through N6-methyladenosine

Fuming Qi1, Wenlong Liu1, Bo Tan1

  • 1Urology Department, Shengli OilField Central Hospital, Dongying, Shandong, China.

Frontiers in Oncology
|January 2, 2023
PubMed

Insights

N6-methyladenosine (m6A) modification down-regulates BTG2 in renal cell carcinoma (RCC), promoting tumor growth. Restoring m6A modification inhibits RCC progression, highlighting BTG2 as a tumor suppressor.

Area of Science:

  • Molecular Biology
  • Oncology
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) mRNA modification regulates gene expression and is implicated in cancer.
  • BTG2 is an anti-proliferative protein that can inhibit tumor progression.

Purpose of the Study:

  • To investigate the role of m6A modification in regulating BTG2 expression in renal cell carcinoma (RCC).
  • To explore the therapeutic potential of targeting m6A modification of BTG2 in RCC.

Main Methods:

  • Analysis of BTG2 expression and m6A levels in RCC tissues.
  • Investigating the interaction between m6A modification, IGF2BP2, and BTG2 mRNA stability.
  • Utilizing CRISPR/dCas13b-METTL3 system to modulate m6A levels of BTG2.

Main Results:

  • BTG2 is frequently downregulated in RCC, correlating with poor prognosis and reduced m6A levels.
  • m6A modification in BTG2's 5'UTR enhances its mRNA stability via IGF2BP2.
  • Targeted m6A hypermethylation of BTG2 significantly inhibits RCC cell proliferation, migration, and induces apoptosis.

Conclusions:

  • BTG2 acts as a tumor suppressor in RCC.
  • m6A modification is a key mechanism for BTG2 silencing in RCC.
  • Modulating BTG2 m6A levels offers a potential therapeutic strategy for RCC.
Keywords:
BTG2Mettl3RCCdCas13bm6A

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