A previous report has revealed that cucurbitacin B (CuB) inhibits cancer cell proliferation and tumorigenesis in non-small cell lung cancer (NSCLC) through epigenetic modifications of several genes. However, whether CuB regulates cell proliferation and apoptosis by altering methylation status of BTG3 in colorectal cancer (CRC) remains unknown. In the present study, the results showed that BTG3 was downregulated in CRC tissues compared with adjacent normal tissues. CuB significantly increased BTG3 levels, induced promoter demethylation, decreased the levels of DNA methyltransferases (DNMT1, DNMT3a and DNMT3b) in both CRC cell lines (SW480 and Caco-2) and the effects of CuB were comparable with those of 5-Aza-dC. We also found that CuB inhibited cell proliferation, accompanied with decreased expression of Ki67. Furthermore, CuB treatment induced cell cycle arrest at G1 phase in SW480 and Caco-2 cells, as well as decreased levels of Cyclin D1 and Cyclin E1. Incubation with CuB promoted cell apoptosis in both CRC cell lines in vitro, accompanied with elevation of cleaved caspase-3 and cleaved PARP. BTG3 knockdown abolished the effects of CuB in CRC cells. In summary, CuB-induced proliferation inhibition and cell apoptosis may be due to the reactivation of BTG3 by promoter demethylation. CuB may be a promising agent for CRC therapy.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.