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Article Abstract
Background/aim: is a key regulator of hepatocellular carcinoma (HCC) progression, that promotes cell adhesion, migration, and activation. However, its transcriptional regulation remains poorly understood. This study aimed to elucidate the role of , a secreted regulator of the signaling pathway, in expression and its functional implications in tumor progression.
Materials And Methods: Public databases (TCGA HCC, GSE271352, GSE271354) and clinical samples from 83 HCC patients at CNUHH were analyzed to investigate the regulation of by and its downstream transcriptional regulator, . Molecular analyses, including qRT-PCR, western blotting, and ChIP assays, were conducted to assess expression and JunB binding at its promoter sites. Functional studies were performed in hepatic cancer cell lines using recombinant LGALS3BP treatment and siRNA-mediated knockdown experiments to evaluate their effects on expression and associated phenotypes.
Results: expression showed a significant positive correlation with and in both TCGA and CNUHH HCC patients. Treatment with recombinant LGALS3BP induced expression by enhancing JunB transcriptional activity. Conversely, knockdown significantly suppressed expression, reducing cell-to-cell adhesion and invasiveness in hepatic cancer cells.
Conclusion: The - axis regulates expression and contributes to HCC progression. Targeting , with as a potential biomarker, and the combined inhibition of both and may represent a promising therapeutic strategy for HCC.
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