ArticleCancer genomics & proteomics
Splicing Factor SF3B4 Promotes Melanoma Migration
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 1 paper.
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Who cites it
1 citing paper in PubMed.
- Anti-gicerin Antibody Suppresses Early Pulmonary Metastatic Colonization of B16F10 Melanoma Cells.In vivo (Athens, Greece)Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimMelanoma is a highly aggressive cancer in which metastatic dissemination remains the primary cause of mortality. This study aimed to define the role of the splicing factor 3b subunit 4 (SF3B4) in melanoma progression and its downstream regulatory mechanisms. MATERIALS AND
methodsSF3B4 expression was analyzed in public datasets. Its functional role was assessed by knockdown or inhibition in melanoma cells using proliferation, wound healing, and transwell assays. Talin1 expression and splicing were evaluated by RT-qPCR and immunoblotting, and FAK phosphorylation was measured as a downstream readout.
resultsSF3B4 is significantly upregulated in melanoma, particularly in metastatic lesions, and its expression correlates with poor patient survival. SF3B4 depletion suppresses melanoma cell growth and migration. Talin1 was identified as a downstream target of SF3B4, as SF3B4 knockdown reduced Talin1 mRNA and protein levels and impaired its splicing, leading to increased intron retention. Consistently, SF3B4 loss reduced phosphorylation of focal adhesion kinase (FAK), indicating attenuation of Talin1-mediated signaling. Talin1 knockdown recapitulated the migration defects observed upon SF3B4 depletion, and combined knockdown showed no additive effect, supporting a shared regulatory pathway.
conclusionSF3B4 promotes melanoma cell migration through splicing-dependent regulation of Talin1. The SF3B4-Talin1 axis represents a potential therapeutic target in metastatic melanoma.
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