Effect of bevacizumab on expression level of GLI1 and ING4 in colon cancer animal model
- Bing Suo
- Caiyu Wu
- Fen Mei
Affiliations: General Hospital of Heilongjiang Province Land Reclamation Bureau, Harbin, Heilongjiang 150088, P.R. China, Department of Medical Laboratory, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, P.R. China
- Published online on: May 28, 2020 https://doi.org/10.3892/ol.2020.11677
Copyright: © Suo
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This study aimed to investigate the effect of bevacizumab on GLI1 and ING4 expression in colon cancer animal model. Colon cancer model in rats was induced by azoxymethane (AOM). Bevacizumab was used for the treatment of colon cancer rats. Tumor volume and weight were measured, tumor growth curve was visualized and tumor inhibition rate was calculated. GLI1 and ING4 of colon cancer cells were silencing expressed. Western blot analysis was used to detect the expressions of GLI1, ING4, caspase‑3, Bax, β‑catenin, Bcl2, PTEN, PI3K, Akt, NF-κB. The apoptosis rate was detected by flow cytometry. MTT assay was used to detect cell activity to get IC50 value. After AOM induced colon cancer model in rats, the expressions of ING4, caspase‑3, Bax and PTEN were downregulated, the expressions of GLI1, β‑catenin, Bcl2, PI3K, Akt and NF‑κB were upregulated and the apoptosis rate was downregulated. After bevacizumab treatment, the tumor volume and weight decreased, the expressions of ING4, caspase‑3, Bax, PTEN were upregulated, the expressions of GLI1, β‑catenin, Bcl2, PI3K, Akt, NF‑κB were downregulated, and the cell apoptosis rate increased. Cell experiments showed that GLI1 promotes tumor growth and reduces the sensitivity of bevacizumab, while ING4 inhibits tumor growth and increases the sensitivity of bevacizumab. Bevacizumab inhibits the growth of colon cancer tumor by upregulating ING4 and downregulating GLI1.