B7H6 silencing enhanced MKN-45 cancer cells' chemosensitivity to 5-fluorouracil

Abstract

Abstract Background Gastrointestinal cancers are a serious health threat on a global scale. Immunotherapeutic methods are also being investigated in this circumstance, and early data from ongoing studies with checkpoint inhibitors such as B7H6 inhibitors is impressive. As a result, we studied the effects of B7H6 suppression on the MKN-45 cancer cell line using particular siRNA and underlying processes when 5-fluorouracil is used (5-FU). Methods B7H6 siRNA and 5-FU were used alone or in combination to treat MKN-45 cells. Following that, the MTT test was used to determine the IC50 of 5-FU and cell viability. The apoptotic induction (using Annexin V / PI) and cell cycle activity were investigated through flow cytometry. The migration of cells was determined with a wound healing test, accordingly. Additionally, we evaluated the clonogenic potential of MKN-45 cells and assessed gene expression in treated groups using qRT-PCR. Results Our findings indicate that silencing B7H6 sensitizes MKN-45 cells to 5-FU treatment by inducing apoptosis and modulating the expression of genes such as Bax, Bcl-2, caspase-3, and MMP3, which are the key mediators of apoptosis. Additionally, both B7H6 silencing and 5-Fu therapy decreased cell migration cooperatively. Moreover, combination treatment stopped the MKN-45 cells' ability to form colonies by stopping the cell cycle in the sub-G1 stage. Conclusion Silencing B7H6 enhanced MKN-45 cells' chemosensitivity to 5-Fu and exerted anti-tumor effects. After completing studies, this technique may be considered an effective therapy option for this malignancy.