Gelsolin Inhibits the Proliferation of Colon Cancer Cells by Enhancing the Expression of TNFR2/CASP10 as a Death Receptor Pathway

Background: Colon cancer has the second highest incidence rate of digestive system tumors. It relies on surgical treatment, radiotherapy and chemotherapy, and targeted drug therapy. Objective: To study the mechanism of GSN in the proliferation of colon cancer cells. Materials and Methods: The expression of gelsolin (GSN) was analyzed with the data of colon cancer patients in the TCGA database. SW620 cells were treated by GSN in vitro and the gene expression was detected by immunoblotting and quantitative PCR. Results: The expression of GSN was found significantly low in colon cancer cells and correlated with the prognosis of patients. The SW620 cell line cultured in vitro was treated with exogenous GSN. SW620 can be significantly inhibited above the concentration of 250 μg/ml. The results of immunoblotting and quantitative PCR showed that exogenous GSN can effectively improve the transcription level of death receptor-related pathway genes such as TNFR2 and CASP10. Conclusion: This study found that GSN inhibited the proliferation of SW620 cells in vitro by upregulating the expression of death receptor pathway-related proteins.