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SF3B4 downregulation restrains lung adenocarcinoma tumorigenesis via 5' alternative splicing of KAT2A

Ailin Qu1, Bo Han2, Mengmeng Hua3,4

  • 1Department of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, 250012, Shandong, China.

Scientific Reports
|January 3, 2024
PubMed

Insights

Aberrant splicing factor SF3B4 promotes lung adenocarcinoma (LUAD) growth by downregulating KAT2A. Targeting the SF3B4/KAT2A axis offers potential therapeutic strategies for LUAD patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Aberrant splicing factor expression is implicated in lung adenocarcinoma (LUAD) pathogenesis.
  • The specific role of SF3B4 in LUAD progression remains incompletely understood.

Purpose of the Study:

  • To investigate the functional impact of SF3B4 on LUAD development.
  • To elucidate the molecular mechanisms underlying SF3B4's role in LUAD.

Main Methods:

  • In vitro assays including apoptosis, proliferation, and migration assays were performed.
  • Gene manipulation techniques were employed to study SF3B4 and KAT2A interactions.
  • RNA and protein levels were analyzed following SF3B4 knockdown.

Main Results:

  • SF3B4 was found to promote LUAD cell growth and tumorigenesis.
  • SF3B4 knockdown induced an alternative splice site in KAT2A's 5'-UTR, reducing KAT2A RNA and protein levels.
  • Decreased KAT2A partially counteracted the tumor-promoting effects of SF3B4.

Conclusions:

  • The SF3B4/KAT2A axis is a critical regulator of LUAD progression.
  • SF3B4 promotes LUAD by downregulating KAT2A expression.
  • This axis presents a potential therapeutic target for lung adenocarcinoma.

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