Wanle Hu 1 , Chenchen Wu 1 , Chenchen Yuan 1 , Minyuan Chen 1 , Chun Jin 1 , Chenguo Zheng 1 . Show Affiliations »
Abstract
Background: Colorectal cancer (CRC) is one of the most common tumors, and its five-year survival is still very low despite of the advance of treatment strategies. The antitumor effect of ethanol extracted from radix of Actinidia chinensis (EERAC) were identified in human colon cancer cells, but the underlying mechanism remains unclear. Methods: Cell proliferation, migration, and invasion were measured with cell counting kit-8 (CCK-8), wound healing, and transwell assays. Cell apoptosis and cycle were detected by flow cytometry. Western blotting and qRT-PCR were used to measure expression of target molecules. Xenograft tumor assay was applied to detect the influence of EERAC on tumor growth. Results: we found that EERAC inhibited the cell viability, migration, and invasion of SW480 cells in a concentration dependent manner, but promoted apoptosis and the cell percentage in S phase significantly. The suppression of notch-signaling pathway molecules, Notch1, Jagged1, and c-Myc, by EERAC was confirmed using western blotting and immunohistochemical staining. The significant inhibition of tumor growth by EERAC was also observed. Meanwhile, EERAC remarkably reversed the effects of mastermind like transcriptional coactivator 1 (MAML1, activator of notch-signaling pathway) on cell survival of SW480. Conclusions: EERAC might be a promising chemotherapeutic agent for CRC treatment. © The author(s).
Background: Colorectal cancer (CRC ) is one of the most common tumors , and its five-year survival is still very low despite of the advance of treatment strategies. The antitumor effect of ethanol extracted from radix of Actinidia chinensis (EERAC) were identified in human colon cancer cells, but the underlying mechanism remains unclear. Methods: Cell proliferation, migration, and invasion were measured with cell counting kit-8 (CCK-8), wound healing, and transwell assays. Cell apoptosis and cycle were detected by flow cytometry. Western blotting and qRT-PCR were used to measure expression of target molecules. Xenograft tumor assay was applied to detect the influence of EERAC on tumor growth. Results: we found that EERAC inhibited the cell viability, migration, and invasion of SW480 cells in a concentration dependent manner, but promoted apoptosis and the cell percentage in S phase significantly. The suppression of notch -signaling pathway molecules, Notch1 , Jagged1 , and c-Myc , by EERAC was confirmed using western blotting and immunohistochemical staining. The significant inhibition of tumor growth by EERAC was also observed. Meanwhile, EERAC remarkably reversed the effects of mastermind like transcriptional coactivator 1 (MAML1 , activator of notch -signaling pathway) on cell survival of SW480 . Conclusions: EERAC might be a promising chemotherapeutic agent for CRC treatment. © The author(s).
Entities: CellLine
Chemical
Disease
Gene
Species
Keywords:
Cell migration; Cell viability; Colorectal cancer; EERAC; Notch-signaling pathway
Year: 2021
PMID: 33403022 PMCID: PMC7778551 DOI: 10.7150/jca.51275
Source DB: PubMed Journal: J Cancer ISSN: 1837-9664 Impact factor: 4.207