【摘 要】
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Objective:Toinvestigatethemechanismofp53-inducedgene3(PIG3)-regulationofradioresistanceinhumannon-smallcelllungcancer(NSCLC)cells,inordertoexplorenewbiomarkersandtherapeutictargetstocombatradioresistanceandimprovethe5-yearsurvivalrate.Methods:ThePIG3genew
【机 构】
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State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protecti
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Objective:To investigate the mechanism of p53-induced gene 3 (PIG3)-regulation of radioresistance in human non-small cell lung cancer (NSCLC) cells, in order to explore new biomarkers and therapeutic targets to combat radioresistance and improve the 5-year survival rate.
Methods:The PIG3 gene was knocked down in A549 cells using siRNA, and was overexpressed in H1299 cells using a PIG3 expression plasmid. After confirming PIG3 knockdown and overexpression through the Western blot analysis, the radiosensitivity, DNA damage, cell cycle distribution, and apoptosis in these cells were analyzed using colony formation assay, immunofluorescence staining for γH2AX, and flow cytometry, respectively.
Results:PIG3 silencing markedly increased the radiosensitivity of NSCLC cells, with radiosensitization ratios of 1.12 and 1.25. Compared with the corresponding negative control, PIG3 knockdown significantly enhanced G2/M phase arrest (siNC: 26.12 ± 2.50, siPIG3#1: 34.98 ± 4.19, siPIG3#2: 37.79 ± 3.53, P
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