ArticleHistology and histopathology2025
Knockdown of TBRG4 suppresses the migration, invasion, and epithelial-to-mesenchymal transition of pancreatic cancer cells via TGF-β/smad3 signaling.
Article in Histology and histopathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Insights into the E2F target genes in breast cancer: associations of pathway genes with prognosis and immune cell filtration based on in silico and ex vivo analyses.Cancer cell international · 2025Article
- Comprehensive analysis of regulatory B Cell related genes in prognosis and therapeutic response in lung adenocarcinoma.Frontiers in immunology · 2025Article
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3 authors.
Funding
Abstract
introductionPancreatic cancer (PC) is one of the deadliest malignancies worldwide, with a low five-year survival rate of less than 10%. Transforming growth factor β regulator 4 (TBRG4) is differentially expressed in PC tissues, but its specific functions and regulatory role in PC have not been clarified.
methodsTBRG4 mRNA expression in PC cells was measured by qRT-PCR. Protein levels of TBRG4, key markers related to the epithelial-mesenchymal transition (EMT) process, and factors related to the TGF-β/smad3 pathway were quantified by western blot. The migratory and invasive abilities of PC cells were evaluated by wound healing and Transwell assays, respectively. Spearman's correlation analysis was performed to analyze the expression correlation between TBRG4 and TGF-β1 (or SMAD3). Xenograft mouse models were established to explore the
resultsThe mRNA and protein expression of TBRG4 were elevated in PC cells. TBRG4 knockdown repressed PC cell migration, invasion, and the EMT process. Moreover, TBRG4 activated TGF-β/smad3 signaling in PC cells and positively correlated with TGF-β1 (or SMAD3) expression in PC tissues based on bioinformatics analysis. Furthermore, SRI-011381 (an agonist of TGF-β1) counteracted the inhibitory influence of TBRG4 knockdown on PC cellular behaviors, and SB431542 (an inhibitor of the TGF-β type I receptor) treatment countervailed the promoting influence of TBRG4 overexpression on PC cell invasion, migration, and EMT. Results of
conclusionThe silencing of TBRG4 inhibits PC cell invasion, migration, EMT, and tumorigenesis by inactivating TGF-β/smad3 signaling.
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