ArticleFrontiers in pharmacology2025
CS-6-induced p62 accumulation exacerbates DNA damage in colorectal cancer.
Article in Frontiers in pharmacology, 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: Gamabufotalin (CS-6), a bufadienolide derived from Chansu, has been reported to exhibit anti-tumor effects in various cancers, including glioblastoma, nonsmall cell lung cancer, and breast cancer. However,its role in colorectal cancer (CRC) remains unexplored. Objective: Our study aimed to evaluate the inhibition of CS-6 to CRC cells by cell viability assay, colony formation assay, comet assay, and cell cycle analysis firstly. And its molecular mechanism was studied by immunofluorescence (IF) assay, western blot (WB) assay, siRNA transfection, protein-protein interaction (PPI) network and co-immunoprecipitation (Co-IP) assay. Finally, the in vivo antitumor assessments of CS-6 on colorectal cancer was validated through an transplant colorectal cancer model. Results: CS-6 treatment significantly inhibited CRC SW620 and DLD1 cell viability and colony formation Conclusion: This study suggests that CS-6 may exert its anti-tumor effects in CRC by inducing autophagy defects, resulting in p62 accumulation and DNA damage
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