敲低B7-H4对MFC细胞增殖和肿瘤形成的影响及其机制OA

OBJECTIVE:To investigate effects of the co-stimulatory molecule B7-H4 on MFC cell proliferation and tumor formation,and to explore its potential mechanisms.METHODS:MFC cells were transfected with lentiviruses to knock down B7-H4 expression,and stable transfection cell lines were screened.The cells were divided into a knockdown group(transfected with B7-H4 knockdown lentivirus)and a control group(transfected with the empty vector lentivirus).Expression levels of B7-H4 mRNA and protein in MFC cells were detected using RT-qPCR and Western blot to evaluate knockdown effects.Impact of B7-H4 knockdown on MFC cell proliferation and migration was assessed through CCK-8 assay and cell scratch experiments.The stably transfected cells from both groups were then injected subcutaneously into mice,and tumor formation was evaluated through tumor transplantation experiments.Expression levels of B7-H4,WNT7A,and STAT3 in MFC cells and mouse tumor tissues were analyzed using RT-qPCR and Western blot.RESULTS:RT-qPCR and Western blot results showed that compared to the control group,expression levels of B7-H4 in the knockdown group were significantly reduced(P<0.01),indicating successful construction of B7-H4 knockdown cell lines.In MFC cells,B7-H4 knockdown significantly reduced both proliferation and migration capacity compared to the control group(P<0.01).In subcutaneous tumor formation experiments,the tumor volume and mass in the knockdown group were significantly smaller than those in the control group(P<0.01).RT-qPCR and Western blot results demonstrated that expression levels of B7-H4,WNT7A,and p-STAT3 in the knockdown group were significantly lower than those in the control group(P<0.01).In contrast,total STAT3 expression showed no significant change(P>0.05).CONCLUSION:B7-H 4 knockdown inhibited MFC cell proliferation and migration and affected tumor formation in MFC cells.Low expression of B7-H4 inhibited expression of WNT7A and STAT3.