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RBM15 silencing promotes ferroptosis by regulating the TGF-β/Smad2 pathway in lung cancer

Jing Feng1, Yaling Li1, Fen He1

  • 1Department of Thoracic Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou City, Guangdong Province, China.

Environmental Toxicology
|January 30, 2023
PubMed
Abstract

Insights

Silencing RNA binding motif protein 15 (RBM15) in lung cancer cells promotes ferroptosis and inhibits tumor growth. This occurs via the TGF-β/Smad2 pathway, offering potential new therapeutic strategies for lung cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • RNA binding motif protein 15 (RBM15) is implicated in various cancers.
  • The role of RBM15 in lung cancer development and its underlying mechanisms require further elucidation.
  • Understanding RBM15's function is crucial for developing targeted lung cancer therapies.

Purpose of the Study:

  • To investigate the function and mechanism of RNA binding motif protein 15 (RBM15) silencing in lung cancer.
  • To determine the impact of RBM15 knockdown on lung cancer cell proliferation, invasion, and migration.
  • To explore the role of RBM15 in regulating ferroptosis and associated signaling pathways in lung cancer.

Main Methods:

  • Cell viability, proliferation, invasion, and migration assays (MTT, EdU, wound healing, transwell) were performed after RBM15 knockdown in A549 and H1299 lung cancer cells.
  • Analysis of lipid peroxidation, labile iron pool (LIP), ferrous iron (Fe2+), and ferroptosis-related gene expression.
  • RNA sequencing (RNA-seq) followed by differential gene expression (DEG), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
  • Western blot to assess RBM15 and pathway-related gene expression.

Main Results:

  • RBM15 is highly expressed in lung cancer cells and its silencing significantly reduced cell viability, proliferation, invasion, and migration.
  • RBM15 silencing increased labile iron pool (LIP), ferrous iron (Fe2+), and lipid peroxidation, indicating promotion of ferroptosis.
  • RNA-seq identified 367 upregulated and 368 downregulated DEGs, enriched in key cellular functions and pathways.
  • RBM15 silencing decreased TGF-β/Smad2 pathway expression, and TGF-β activator reversed the inhibitory effects.

Conclusions:

  • RBM15 silencing promotes ferroptosis in lung cancer cells through the TGF-β/Smad2 pathway.
  • Inhibition of RBM15 suppresses lung cancer cell growth and tumor progression.
  • Targeting RBM15 offers a promising therapeutic strategy for lung cancer treatment.
Keywords:
RBM15Smad2TGF-βferroptosislung cancer

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