Autor: |
chao Huang, Haosheng liu, Yidian Yang, Yue He, Weizeng shen |
Jazyk: |
angličtina |
Rok vydání: |
2024 |
Předmět: |
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Zdroj: |
Heliyon, Vol 10, Iss 16, Pp e36059- (2024) |
Druh dokumentu: |
article |
ISSN: |
2405-8440 |
DOI: |
10.1016/j.heliyon.2024.e36059 |
Popis: |
Objective: To explore the mechanisms of the TGF-β1/Smad and NF-κB pathways in the effect of berberine (BBR) on colon cancer epithelial–mesenchymal transition (EMT) and their regulatory relationships with microRNAs (miRNAs). Methods: TGF-β1 was used to induce EMT in normal colon epithelial HCoEpiC cells and colon cancer HT29 cells in vitro. After BBR intervention, the expression of EMT-related markers and the major molecules involved in the TGF-β1/Smad and NF-κB pathways were detected via western blotting. Cell migration was detected via wound healing assays. SMAD2 and NF-κB p65 were overexpressed and transfected into cells, and the inhibitors SB431542 and BAY 11–7082 were added to block the TGF-β1/Smad and NF-κB pathways, respectively. The mRNA expression levels of related microRNA genes were detected by using RT‒PCR. Results: Treatment with 10 ng/ml TGF-β1 for 72 h significantly induced EMT in HCoEpiC and HT29 cells, which was repressed by BBR. BBR significantly inhibited the TGF-β1-induced migration of HCoEpiC and HT29 cells and the TGF-β1-promoted expression of p-Smad2/3, NF-κB p65, and p-IκBα. Compared to those in the group treated with TGF-β1, the expression of NF-κB p65 and p-Smad2 in the group treated with NF-κB pathway inhibitor BAY 11–7082 was decreased (P |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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