AI Article Synopsis
- This study investigates the role of the transcriptional coactivator CBP in hepatocellular carcinoma (HCC) and evaluates how PRI-724, a selective inhibitor, affects this cancer type.
- Researchers analyzed 199 HCC samples and treated cell lines with PRI-724, finding that nuclear β-catenin expression was linked to larger tumors and that PRI-724 significantly inhibited cell growth.
- Results suggest that PRI-724 (C-82) could serve as a potential therapeutic option for HCC patients with β-catenin activation by increasing cell cycle arrest and promoting apoptosis.
Article Abstract
Background/aim: CBP is a transcriptional coactivator in the Wnt/β-catenin pathway that is related to cell kinetics and differentiation. This study aimed to characterize β-catenin-activated hepatocellular carcinoma (HCC) and evaluate the direct effects of PRI-724 (a selective inhibitor of Wnt/β-catenin/CBP signaling) on HCC.
Materials And Methods: Immunohistochemistry for β-catenin was performed in 199 HCC resected samples. Moreover, using cultured HCC cell lines, cell kinetics and its related proteins were analyzed after treatment of cells with C-82 (active form of PRI-724).
Results: Nuclear β-catenin expression was found in 18% of HCC cases and the tumor sizes in these positive samples were larger. In HCC cell lines with a constitutively activated β-catenin, C-82 inhibited cell proliferation. C-82 led to an increase in the percentage of cells in the G/G phase of the cell cycle. The percentage of cells in the sub-G phase also increased. Moreover, C-82 treatment significantly decreased the expression of cell proliferating markers and increased the expression of apoptosis-related proteins.
Conclusion: PRI-724(C-82) may be a novel drug for β-catenin-activated HCC therapy.
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| http://dx.doi.org/10.21873/anticanres.14524 | DOI Listing |
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