Exploration of the mechanism by which erianin remodels chemotherapeutic response in colorectal cancer
Ai Lianjie
Sun Zhifu
Lu Weiyuan
Abstract:Objective To explore the mechanism by which erianin remodels chemotherapeutic response in colorectal cancer.Methods Human colorectal cancer cell lines HCT116 and SW480 were used as research objects and divided into blank control group(only normal medium added),oxaliplatin group(10 μmol/L oxaliplatin added),erianin groups(0,25,50 nmol/L erianin added),and combination group(10 μmol/L oxaliplatin+50 nmol/L erianin added).Cell counting kit assay was used to detect cell viability and calculate half-maximal inhibitory concentration(IC50);colony formation assay was performed to evaluate cell proliferation ability;flow cytometry was used to assess cell apoptosis rate and cell cycle distribution;relevant kits were employed to determine lipid peroxidation level,glutathione and malondialdehyde levels;Western blot was used to detect the expression of ferroptosis-related proteins[glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11),long-chain acyl-CoA synthetase 4(ACSL4)].Results For HCT116 and SW480 cells,increased erianin concentration and prolonged treatment time both gradually reduced cell viability,and the cell viability in the 50 nmol/L erianin treatment group was significantly lower than that in the 25 nmol/L treatment group(P<0.05).The 48 h IC50 values of erianin for HCT116 and SW480 cells were 30.2 nmol/L and 101.4 nmol/L,respectively.The colony formation rate,glutathione content,and protein levels of GPX4 and SLC7A11 in the single-drug treatment groups(oxaliplatin group and erianin group)were significantly lower than those in the blank control group,and the relevant indicators in the combination group were the lowest,which were further decreased compared with the single-drug treatment groups(all P<0.05).The cell apoptosis rate,lipid peroxidation level,malondialdehyde content,and ACSL4 protein level in the single-drug treatment groups were significantly higher than those in the blank control group,and the relevant indicators in the combination group were the highest,which were further increased compared with the single-drug treatment groups(all P<0.05).Compared with the blank control group,both the oxaliplatin group and the erianin group induced G2/M phase arrest;the proportion of G2/M phase cells in the combination group was further increased,while the proportions of S phase and G0/G1 phase cells were decreased(all P<0.05).Conclusion Erianin can inhibit the viability of colorectal cancer cells,and its combination with oxaliplatin can enhance the inhibitory effect.The mechanism may be related to inducing cell apoptosis,arresting cell cycle,and promoting ferroptosis.
Keywords:Colorectal cancerErianinOxaliplatinChemotherapeutic responseCell apoptosisFerroptosis
Publication Date:2026-01-18
Online Publishing Date:2026-09-14(First online date of this platform, not the publication date of the document)
Pages:5( 78-82 )
