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Title:
Suppressive effect of α-mangostin for cancer stem cells in colorectal cancer via the Notch pathway | BMC Cancer
Description:
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. α-mangostin (αM) has been confirmed to have antiproliferative and apoptotic effects on cancer cells. This study aimed to evaluate the selective inhibition of αM 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 αM. A sphere forming assay and flow cytometry with CSC markers were carried out to evaluate the αM-mediated inhibition of CSCs. Western blot analysis and quantitative real-time PCR were performed to investigate the effects of αM on the Notch signaling pathway and colon CSCs. The in vivo anticancer efficacy of αM in combination with 5-FU was investigated using a xenograft mouse model. Results αM inhibited the cell viability and reduced the number of spheres in HT29 and SW620 cells. αM treatment decreased CSCs and suppressed the 5-FU-induced an increase in CSCs on flow cytometry. αM markedly suppressed Notch1, NICD1, and Hes1 in the Notch signaling pathway in a time- and dose-dependent manner. Moreover, αM 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 αM group and in the αM group with 5-FU treatment. Conclusion This study shows that low-dose αM inhibits CSCs in CRC and suppresses 5-FU–induced augmentation of CSCs via the Notch signaling pathway.
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Keywords {🔍}
cells, cancer, pubmed, article, cell, notch, google, scholar, cscs, treatment, cas, fig, signaling, stem, group, crc, assay, colorectal, central, effect, pathway, kim, hes, data, usa, significantly, effects, viability, korea, control, treated, tumor, csc, anticancer, fuinduced, colon, decreased, dapt, republic, hey, min, results, increase, alphamangostin, moon, proportion, compared, flow, agents, university,
Topics {✒️}
yeung-chul mun article google scholar seung-yong seo directed cd44/cd133 double-positive tumors quantitative real-time pcr cd133-pe double-positive cells article download pdf young-ho anh participated sung-ae jung alpha-mangostin attenuates stemness phenylglycine-t-butyl ester seung-yong seo tae il kim novo-cyte flow cytometer young-ho ahn ji-hee kwon retinaldehyde-dependent aldh assay human colon cancer notch signal pathway γ-secretase inhibitor dapt antioxid redox signal suppresses 5-fu–induced augmentation young-ho anh alpha-mangostin induces apoptosis national research foundation promising adjunctive agent mitochondrial-mediated apoptosis cd133+cd44+ cells compared cancer cell invasion anti-skin cancer properties cd133+cd44+ cells increased induce colon adenoma caspase-dependent apoptosis induction characteristics including proliferation eun ju kim full access privacy choices/manage cookies metastatic colon cancer stem cell investig breast cancer cells highly conserved pathway cell cycle arrest professor sy seo cervical cancer stem cell counting kit-8 αm-mediated inhibition western blot showing lumino image analyzer apoptotic cell death cancer cell viability
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headline:Suppressive effect of α-mangostin for cancer stem cells in colorectal cancer via the Notch pathway
description: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. α-mangostin (αM) has been confirmed to have antiproliferative and apoptotic effects on cancer cells. This study aimed to evaluate the selective inhibition of αM on CSCs in colorectal cancer (CRC) and the suppressive effect on 5-fluorouracil (5-FU)-induced CSCs. The cell viability assay was performed to determine the optimal concentration of αM. A sphere forming assay and flow cytometry with CSC markers were carried out to evaluate the αM-mediated inhibition of CSCs. Western blot analysis and quantitative real-time PCR were performed to investigate the effects of αM on the Notch signaling pathway and colon CSCs. The in vivo anticancer efficacy of αM in combination with 5-FU was investigated using a xenograft mouse model. αM inhibited the cell viability and reduced the number of spheres in HT29 and SW620 cells. αM treatment decreased CSCs and suppressed the 5-FU-induced an increase in CSCs on flow cytometry. αM markedly suppressed Notch1, NICD1, and Hes1 in the Notch signaling pathway in a time- and dose-dependent manner. Moreover, αM 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 αM group and in the αM group with 5-FU treatment. This study shows that low-dose αM inhibits CSCs in CRC and suppresses 5-FU–induced augmentation of CSCs via the Notch signaling pathway.
datePublished:2022-03-29T00:00:00Z
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Cancer stem cell
Colorectal cancer
Notch signal
Phytochemical agent
α-Mangostin
Cancer Research
Oncology
Surgical Oncology
Health Promotion and Disease Prevention
Biomedicine
general
Medicine/Public Health
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headline:Suppressive effect of α-mangostin for cancer stem cells in colorectal cancer via the Notch pathway
description: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. α-mangostin (αM) has been confirmed to have antiproliferative and apoptotic effects on cancer cells. This study aimed to evaluate the selective inhibition of αM on CSCs in colorectal cancer (CRC) and the suppressive effect on 5-fluorouracil (5-FU)-induced CSCs. The cell viability assay was performed to determine the optimal concentration of αM. A sphere forming assay and flow cytometry with CSC markers were carried out to evaluate the αM-mediated inhibition of CSCs. Western blot analysis and quantitative real-time PCR were performed to investigate the effects of αM on the Notch signaling pathway and colon CSCs. The in vivo anticancer efficacy of αM in combination with 5-FU was investigated using a xenograft mouse model. αM inhibited the cell viability and reduced the number of spheres in HT29 and SW620 cells. αM treatment decreased CSCs and suppressed the 5-FU-induced an increase in CSCs on flow cytometry. αM markedly suppressed Notch1, NICD1, and Hes1 in the Notch signaling pathway in a time- and dose-dependent manner. Moreover, αM 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 αM group and in the αM group with 5-FU treatment. This study shows that low-dose αM inhibits CSCs in CRC and suppresses 5-FU–induced augmentation of CSCs via the Notch signaling pathway.
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Colorectal cancer
Notch signal
Phytochemical agent
α-Mangostin
Cancer Research
Oncology
Surgical Oncology
Health Promotion and Disease Prevention
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general
Medicine/Public Health
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name:Department of Internal Medicine & Inflammation-Cancer Microenvironment Research Center, College of Medicine, Ewha Womans University, Seoul, South Korea
name:Department of Internal Medicine & Inflammation-Cancer Microenvironment Research Center, College of Medicine, Ewha Womans University, Seoul, South Korea
name:Inflammation-Cancer Microenvironment Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea
name:Department of Pharmacology, College of Medicine, Ewha Womans University, Seoul, Republic of Korea
name:Department of Internal Medicine & Inflammation-Cancer Microenvironment Research Center, College of Medicine, Ewha Womans University, Seoul, South Korea
name:Inflammation-Cancer Microenvironment Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea
name:Department of Molecular Medicine, College of Medicine, Ewha Womans University, Seoul, Republic of Korea
name:College of Pharmacy, Gachon University, Incheon, Republic of Korea
name:Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea
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