Silent information regulator 2 promotes clear cell renal cell carcinoma progression through deacetylation and small ubiquitin-related modifier 1 modification of glucose 6-phosphate dehydrogenase.
Silent information regulator 2 promotes clear cell renal cell carcinoma progression through deacetylation and small ubiquitin-related modifier 1 modification of glucose 6-phosphate dehydrogenase.
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沉默信息调节因子2通过葡萄糖6-磷酸脱氢酶的去乙酰化和小泛素相关修饰因子1修饰促进透明细胞肾细胞癌的进展。
DOI：
10.1111/cas.15085
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发表时间：
2021-10
期刊：
影响因子：
5.7
通讯作者：
Zhu Y
中科院分区：
文献类型：
--
作者：
Ni Y;Yang Z;Agbana YL;Bai H;Wang L;Yang L;Yi Z;Cheng J;Zhang Q;Kuang Y;Zhu Y
透明细胞肾细胞癌 (ccRCC) 中沉默信息调节因子 2 (SIRT2) 和葡萄糖 6-磷酸脱氢酶 (G6PD) 之间的调节关系仍不清楚。本研究旨在探讨SIRT2在ccRCC中的功能及其对G6PD的调节作用。首先分析了 SIRT2 的癌症基因组图谱数据挖掘。定量实时 PCR 和蛋白质印迹分析分别用于评估 mRNA 和蛋白质表达水平。使用细胞活力、集落形成、细胞周期、细胞凋亡以及TUNEL测定和EdU染色来研究SIRT2在ccRCC增殖和凋亡中的作用。使用免疫共沉淀 (Co-IP) 分析分析 ccRCC 细胞中 SIRT2 和 G6PD 之间的关联。定量 Co-IP 检测用于检测 G6PD 泛素化和小泛素相关修饰物 1 (SUMO1) 的水平。还进行了体内实验以证实体外研究结果。结果表明SIRT2通过调节细胞周期和凋亡相关蛋白促进ccRCC增殖并抑制细胞凋亡。沉默信息调节因子2与G6PD相互作用，通过脱乙酰化促进其活性，并通过减少其泛素化和增强其SUMO1修饰来增加其稳定性。沉默信息调节因子2也促进体内ccRCC肿瘤的发展。综上所述，本研究表明 SIRT2 通过增加 G6PD 活性和稳定性来促进 ccRCC 进展，可能成为 ccRCC 潜在的新诊断和治疗靶点。本研究探讨透明细胞肾细胞癌（ccRCC）中沉默信息调节因子2（SIRT2）的功能及其对葡萄糖6-磷酸脱氢酶的调节作用。旨在为ccRCC患者的靶向治疗提供新的分子线索。该研究支持 SIRT2 在 ccRCC 中的致癌作用，并且 SIRT2 可能是 ccRCC 的潜在治疗靶点。
The regulatory relationship between silent information regulator 2 (SIRT2) and glucose 6‐phosphate dehydrogenase (G6PD) in clear cell renal cell carcinoma (ccRCC) is still unclear. The present study aimed to explore the function of SIRT2 and its regulatory effect on G6PD in ccRCC. The Cancer Genome Atlas data mining of SIRT2 was first analyzed. Quantitative real‐time PCR and western blot analyses were used to assess the mRNA and protein expression levels, respectively. Cell viability, colony formation, cell cycle, cell apoptosis, and TUNEL assays and EdU staining were used to investigate the roles of SIRT2 in ccRCC proliferation and apoptosis. The coimmunoprecipitation (Co‐IP) assay was used to analyze the association between SIRT2 and G6PD in ccRCC cells. Quantitative Co‐IP assay was used to detect the levels of G6PD ubiquitination and small ubiquitin‐related modifier 1 (SUMO1). An in vivo experiment was also carried out to confirm in vitro findings. The results indicated that SIRT2 promoted ccRCC proliferation and inhibited apoptosis by regulating cell cycle and apoptosis related proteins. Silent information regulator 2 interacted with G6PD, facilitated its activity through deacetylation, and increased its stability by reducing its ubiquitination and enhancing its SUMO1 modification. Silent information regulator 2 also promoted ccRCC tumor development in vivo. Taken together, the present study indicated that SIRT2 promoted ccRCC progression by increasing G6PD activity and stability, and it could be a potential new diagnostic and therapeutic target for ccRCC. The present study explores the function of silent information regulator 2 (SIRT2) and its regulatory effect of on glucose 6‐phosphate dehydrogenase in clear cell renal cell carcinoma (ccRCC). It aims to provide new molecular clues for targeted treatment of patients with ccRCC. The study supports an oncogenic role for SIRT2 in ccRCC and SIRT2 might be a potential therapeutic target for ccRCC.
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