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Article Abstract
Objective: This study aimed to investigate the role of Kindlin-2 in HCC and its underlying molecular mechanisms, focusing on its regulation of the Fas/FasL signaling pathway.
Materials And Methods: In vitro, Hep3B and HepG2 cells were treated with Kindlin-2 siRNA, a Fas activator, and a combination of Kindlin-2 siRNA and Fas siRNA. Cell proliferation, apoptosis, and cell cycle progression were evaluated using CCK-8 assays and flow cytometry, while the expression of associated proteins was analyzed through Western blotting. In vivo, a nude mouse xenograft model was established, and the expression levels of apoptosis and cell cycle proteins were assessed using Western blotting and immunohistochemistry.
Results: Silencing Kindlin-2 significantly upregulated the expression of Fas and Fas ligand (FasL), activating the Fas/FasL signaling pathway. This activation promoted the recruitment of FADD, leading to the activation of caspase-8 and caspase-3, inducing apoptosis and causing G1 phase cell cycle arrest.
Discussion And Conclusion: This study revealed that Kindlin-2 inhibited apoptosis in HCC by negatively regulating the Fas/FasL signaling pathway. Kindlin-2 reduced apoptosis in HCC cells by suppressing the activation of the Fas/FasL pathway, thereby promoting tumor progression.
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| http://dx.doi.org/10.1080/08923973.2025.2506696 | DOI Listing |
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