STC1对胶质瘤细胞放射敏感性和辐射诱导免疫原性细胞死亡的影响及其机制的初步探究

Objective :By detecting the changes of phenotype, radiosensitivity and immunogenic cell death of glioma cells after knocking out STC1 gene and ionizing radiation treatment, the effect and mechanism of STC1 on radiation-induced immunogenic cell death of glioma were preliminarily explored.Methods :Western blot detected protein expression in cells. The qPCR was used to detect the expression level of mRNA in cells. CCK-8 assay was used to detect the proliferation of glioma cells. The radiosensitivity of gliomas was detected by cloning assay. Flow cytometry was used to detect the cell cycle distribution, apoptosis and exposure of calreticulin and CD47 on the surface of glioma cells after irradiation. Cellular immunofluorescence assay was used to detect the formation of lipid droplets in glioma cellsand the exposure of calreticulin on the surface of glioma cell membrane after irradiation.Results : Knockout of STC1 inhibited the proliferation activity of glioma cells, promoted the apoptosis of glioma cells, aggravated cell cycle arrest, enhanced the radiosensitivity of glioma cells, significantly reduced the number and size of lipid droplets in hypoxic glioma cells, increased the exposure of calreticulin on the surface of glioma cell membrane induced by radiation, and reduced the expression of CD47 on the surface of glioma cell membrane induced by radiation.Conclusion : Knockout of STC1 inhibits the malignant progression of glioma cells, enhances their radiosensitivity, and promotes immunogenic cell death induced by ionizing radiation. The mechanism may be related to the fact that knockout of STC1 aggravates apoptosis induced by ionizing radiation, increases the exposure of \' eat me \' signal calreticulin on the surface of glioma cells, and reduces the expression of \' don \'t eat me \' signal CD47.