ArticleWorld journal of gastrointestinal oncology2025
Transcription factor 3 enhances hepatocellular carcinoma metastasis by upregulating matrix metalloproteinase-11.
Article in World journal of gastrointestinal oncology, 2025. 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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1 citing paper in PubMed.
- Hepatocellular carcinoma metastasis-immune microenvironment crosstalk: emerging mechanisms and immunotherapy.Cellular & molecular biology letters · 2026Review
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4 authors.
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Abstract
backgroundTranscription factor 3 (TCF3) has a vital role in tumor occurrence and progression. However, the specific functions and underlying mechanisms of dysregulated TCF3 in hepatocellular carcinoma (HCC) have not been not thoroughly characterized. Thus, we explored the roles of TCF3 in HCC.
aimTo explore the roles of TCF3 in HCC.
methodsTCF3 knockdown and overexpression models were developed
resultsTCF3 levels were markedly elevated in HCC samples and correlated with poor prognosis. Furthermore, overexpression of TCF3 promoted HCC cell invasion as well as migration, while TCF3 knockdown repressed HCC cell growth. In addition, TCF3 interacted with the promoter region of matrix metalloproteinase-11 (MMP11), facilitating the transcriptional activation of MMP11 mRNA, which consequently enhanced the expression of MMP11. MMP11 knockdown repressed TCF3-associated HCC cell migration and invasion, while its overexpression attenuated the TCF3 knockdown-mediated repression of HCC growth. In human-derived HCC samples, TCF3 was positively correlated with MMP11 expression levels.
conclusionTCF3 was significantly upregulated in HCC. TCF3 overexpression enhanced HCC cell invasion and metastasis through transactivation of MMP11 expression. TCF3 could be a prognostic biomarker and regulator of HCC metastasis.
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