Suppressive effect of alpha-mangostin for cancer stem cells in colorectal cancer via the Notch pathway
- Authors
- Jo, Min Kyoung; Moon, Chang Mo; Kim, Eun Ju; Kwon, Ji-Hee; XIANG, FEI; Kim, Seong-Eun; Jung, Sung-Ae; Kim, Minsuk; Mun, Yeung-Chul; Ahn, Young-Ho; Seo, Seung-Yong; Kim, Tae Il
- Issue Date
- Mar-2022
- Publisher
- BMC
- Keywords
- Cancer stem cell; Colorectal cancer; Notch signal; Phytochemical agent; alpha-Mangostin
- Citation
- BMC CANCER, v.22, no.1
- Journal Title
- BMC CANCER
- Volume
- 22
- Number
- 1
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/84055
- DOI
- 10.1186/s12885-022-09414-6
- ISSN
- 1471-2407
- Abstract
- Background: Since colon cancer stem cells (CSCs) play an important role in chemoresistance and in tumor recurrence and metastasis, targeting of CSCs has emerged as a sophisticated strategy for cancer therapy. alpha-mangostin (alpha M) has been confirmed to have antiproliferative and apoptotic effects on cancer cells. This study aimed to evaluate the selective inhibition of alpha M on CSCs in colorectal cancer (CRC) and the suppressive effect on 5-fluorouracil (5-FU)-induced CSCs. Methods: The cell viability assay was performed to determine the optimal concentration of alpha M. A sphere forming assay and flow cytometry with CSC markers were carried out to evaluate the alpha M-mediated inhibition of CSCs. Western blot analysis and quantitative real-time PCR were performed to investigate the effects of alpha M on the Notch signaling pathway and colon CSCs. The in vivo anticancer efficacy of alpha M in combination with 5-FU was investigated using a xenograft mouse model. Results: alpha M inhibited the cell viability and reduced the number of spheres in HT29 and SW620 cells. alpha M treatment decreased CSCs and suppressed the 5-FU-induced an increase in CSCs on flow cytometry. alpha M markedly suppressed Notch1, NICD1, and Hes1 in the Notch signaling pathway in a time- and dose-dependent manner. Moreover, alpha M attenuated CSC markers CD44 and CD133, in a manner similar to that upon DAPT treatment, in HT29 cells. In xenograft mice, the tumor and CSC makers were suppressed in the alpha M group and in the alpha M group with 5-FU treatment. Conclusion: This study shows that low-dose alpha M inhibits CSCs in CRC and suppresses 5-FU-induced augmentation of CSCs via the Notch signaling pathway.
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