ArticleCancer genomics & proteomics
SF3B4 Regulates Cellular Senescence and Suppresses Therapy-induced Senescence of Cancer Cells.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Accelerated biological aging: the role of chronic inflammation, weathering and novel therapeutic strategies.Frontiers in aging · 2026Review
- Multi-omics analyses develop and validate the optimal prognostic model on overall survival prediction for resectable hepatocellular carcinoma.Journal of gastrointestinal oncology · 2025Article
- SF3B4 regulates proliferation and apoptosis in hepatocellular carcinoma via alternative splicing and interaction with TRIM28 and SETD5.Journal of translational medicine · 2025Article
- Splicing Factor SF3B4 Promotes Melanoma MigrationCancer genomics & proteomicsArticle
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimCellular senescence is a state in which cells permanently exit the cell cycle, preventing tumor growth, but it can also contribute to aging and chronic inflammation. Senescence induced by cancer therapies, known as therapy-induced senescence (TIS), halts cancer cell proliferation and prevents metastasis. TIS has been investigated as an important therapeutic approach that could minimize cytotoxicity effects. This study aimed to elucidate the role of splicing factor 3B subunit 4 (SF3B4) in cellular senescence and TIS in cancer cells. MATERIALS AND
methodsβ-galactosidase staining was used to examine senescence induction. SF3B4 and p21 expression were determined by RT-qPCR and western blot. Cell proliferation and cell death were evaluated.
resultsSF3B4 expression decreases in replicative senescent human fibroblasts and its knockdown induces senescence via a p21-dependent pathway. In A549 non-small cell lung cancer (NSCLC) cells, SF3B4 knockdown also increased senescence markers. Notably, SF3B4 overexpression mitigated doxorubicin-induced senescence in A549 cells.
conclusionSF3B4 regulates senescence, and this study highlights its potential as a therapeutic target for developing better cancer treatment strategies by leveraging TIS to suppress tumor growth and enhance treatment efficacy.
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Registered trials
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