KLF7/VPS35 axis contributes to hepatocellular carcinoma progression through CCDC85C-activated β-catenin pathway

Abstract Objective Dysregulation of KLF7 participates in the development various cancers, but it is unclear whether there a link between HCC and aberrant expression KLF7. The aim this study was to investigate role proliferation migration hepatocellular carcinoma (HCC) cells. Methods CCK8, colony growth, transwell, cell cycle analysis apoptosis detection were performed explore effect KLF7, VPS35 Ccdc85c on function vitro. Xenografted tumor growth used assess vivo Chip-qPCR luciferase reporter assays applied check regulated at transcriptional manner. Co-IP assay detect interaction Ccdc85c. Immunohistochemical staining qRT-PCR human sampels clinical significance β-catenin. Results Firstly, highly expressed samples correlated with patients’ differentiation metastasis status. overexpression contributed invasion cells vitro vivo. activation necessary for metastasis. Further, co-IP studies revealed that could interact Rescue confirmed knockdown abolished VPS35-medicated promotion invasion. Finally, KLF7/VPS35 axis Ccdc85c, which involved β-catenin signaling pathway, using inhibitor, GK974. Functional suggested downregulation partly reversed capacity cells, by upregulation. Lastly, positive correlation among active-β-catenin patients. Conclusion We demonstrated promoted progression activating Ccdc85c-medicated pathway. Targeting signal might be potential treatment strategy HCC.