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首页> 外文期刊>Journal of Cellular Physiology >Gadd45a gene silencing by RNAi promotes cell proliferation and inhibits apoptosis and senescence in skin squamous cell carcinoma through the p53 signaling pathway
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Gadd45a gene silencing by RNAi promotes cell proliferation and inhibits apoptosis and senescence in skin squamous cell carcinoma through the p53 signaling pathway

机译：Gadd45a RNAi促进细胞基因沉默增殖和抑制细胞凋亡衰老皮肤鳞状细胞癌通过p53信号通路

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摘要

Skin squamous cell carcinoma (SCC) is generally considered as nonaggressive lesions and mainly caused by ultraviolet (UV) radiation. Gadd45a is a key component protecting skin against UV‐induced tumors. For that, the study aims to investigate the mechanism of Gadd45a gene silencing on cell proliferation, apoptosis, and senescence in nude mice with skin SCC through the p53 signaling pathway. Healthy nude mice was collected as the normal group and 40 nude mouse models of skin SCC were successfully established as the model group, which were sub‐divided into five groups. The incidence, size, and weight of SCC tumor of nude mice were observed. The mRNA expression of Gadd45a, Cyclin B1, MMP‐2, Bcl‐2, and Bax were determined by RT‐qPCR. Cell viability, cell cycle and apoptosis, cell senescence were detected by MTT assay, flow cytometry, and β‐galactosidase staining, respectively. The levels of inflammatory factors and vascular endothelial growth factor (VEGF) were detected by using ELISA. The protein expression rate of mutant p53 was detected by immunohistochemistry. Mice transfected with siGadd45a showed increased tumor incidence, size, and weight. Cells transfected with siGadd45a showed decrease in expression of Gadd45a and Bax; and increase in expression of Cyclin B1, MMP‐2, and Bcl‐2, expression of mutant p53, IL‐1α, IL‐1β, IL‐6, TNF‐α, and VEGF. Cell apoptosis and senescence were inhibited, while cell viability and proliferation were promoted after siGadd45a treatment. The results reveal that Gadd45a silencing increases tumor cell proliferation and reduces apoptosis and senescence through the p53 signaling pathway in skin SCC.
机译：皮肤鳞状细胞癌(SCC)一般视为非主动病变,主要由紫外(UV)辐射引起的。保护皮肤免受一个关键组件紫外线诱导的肿瘤。调查Gadd45a基因的机制沉默在细胞增殖、凋亡和衰老在裸小鼠皮肤鳞状细胞癌p53信号通路。收集正常组和40裸鼠皮肤鳞状细胞癌模型成功建立模型组、辅助分成五组。鳞状细胞癌肿瘤的裸鼠实验观察。Gadd45a的表达、细胞周期蛋白B1、MMP 2,应承担Bcl高2和伯灵顿由RT qPCR应承担的决定。生存能力,细胞周期和细胞凋亡,细胞衰老被MTT测定发现,流血细胞计数和β牛乳糖应承担的染色,分别。和血管内皮生长因子(VEGF)用ELISA检测。发现突变型p53的表达率免疫组织化学。siGadd45a显示肿瘤发生率增加,大小,和体重。显示减少的表达Gadd45a和伯灵顿;和细胞周期蛋白B1表达增多,MMP 2,应承担的和Bcl 2突变型p53的表达IL 1α,应承担的IL高1β在IL 6、应承担的肿瘤坏死因子α应承担和VEGF。衰老被抑制,而细胞的可行性和扩散siGadd45a后得到晋升治疗。沉默会增加肿瘤细胞增殖减少细胞凋亡,通过p53衰老信号通路在皮肤鳞状细胞癌。

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