ArticlePeerJ2025
Effect of modulating the extracellular matrix cross linkage by genipin on tumor cell resistance and survival in thioacetamide-induced hepatocellular carcinoma in rats.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Previous studies on patients and rats with hepatocellular carcinoma (HCC) have shown significant changes in the extracellular matrix (ECM). Versican, a component of the ECM, forms extensive multimolecular interactions with other ECM components, particularly hyaluronan, through specific domains in its core protein. However, disturbances in the hyaluronan-versican interaction may affect cancer development. We aimed to examine the effect of modulating matrix cross-linkage between hyaluronan and versican using genipin on tumor cell survival, resistance, and renewal. Methods: Following the induction of HCC in rats using thioacetamide, an oral dose of 10 mg/kg of genipin was administered. Liver impairment was evaluated by measuring serum α-fetoprotein (AFP) levels and examining liver sections stained with hematoxylin/eosin and anti-versican and anti-fibronectin antibodies. Additionally, hepatic expression levels of mRNA and proteins, including epidermal growth factor (EGF), epidermal growth factor receptor (EGFR), fibronectin, glycogen synthase kinase-3 beta (GSK-3β), protein kinase B (PKB), and versican, were analyzed. Results: Genipin enhances rats' survival, leading to reduction in serum AFP levels and number of hepatic nodules. Micro-imaging examinations reveal that genipin reduces vacuolated cytoplasm, apoptotic nuclei, and necrotic nodules. Additionally, it significantly lowers EGF, EGFR, fibronectin, GSK-3β, PKB, and versican expression levels. Conclusion: Genipin may be considered novel anticancer agent with hepatoprotective effects. This is achieved by reducing versican-free forms. Additionally, genipin decreases tumor cells' resistance by lowering the expression of EGF, EGFR, PKB, and GSK-3β. Finally, it reduces tumor cell survival by decreasing the expression of fibronectin.
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