Sh-PLCε Increases The Effects Of Interleukin-2 In Renal Cell Carcinoma Via Fas/Fasl Signaling Pathway

Objective: To explore the role of PLCε in renal cell carcinoma.To study the role of IL-2 in kidney cancer.To investigate whether PLCε plays a role in treatment of IL-2 in renal cell carcinoma.Methods: The Cancer Genome Atlas database was used to analyze the expression levels of Fas and FasL in patients with renal cancer.Immunohistochemistry was used to detect the expression of Fas,FasL,and PLCεin renal cancer tissues.PLCε was knocked down in 786-o and caki using a lentiviral short hairpin RNA(shRNA)。Western blotting was used to measure levels of PLCε,Fas,FasL,Fas-associated protein with death domain(FADD),caspase-8,caspase-3,c-Flip,and tumor necrosis factor receptor-associated factor 2(TRAF-2).MTT assays were used to determine the effects of IL-2 on cell viability.Flow cytometry,4′,6-diamidino-2-phenylindole staining was used to detected apoptosis.T-cell viability was measured by trypan blue staining.Results: Fas,FasL,and PLCε expression levels were increased in renal cancer tissues compared with those in adjacent tissues.PLCε knockdown decreased the expression of Fas,FasL and increased the proportion of apoptoticcells,as demonstrated by caspase-8/caspase-3 pathway analysis.IL-2 treatment increased the expression levels of c-Flip/TRAF-2 in 786-o and caki.In contrast,treatment of cell lines with IL-2 and sh-PLCε to knockdown PLCε increased caspase-8/caspase-3 expression,thereby enhancing apoptosis rates.Conclusions: Knockdown of PLCε promoted the caspase-8/caspase-3apoptotic signal pathway and improved the effects of IL-2 in renal cancer cells.