PTGS2调控细胞增殖及抗氧化能力影响结肠癌患者预后. (Chinese)

PTGS2 affects prognosis of colon cancer patients through regulation of cell proliferation and antioxidant capacity. (English)

Objective To investigate the effect and potential molecular mechanism of PTGS2 on the prognosis of colon cancer patients. Methods The transcriptomic and proteomic data of pan-cancer were collected from TCGA, HPA, UALCAN and other databases, and the expression pattern and prognostic value of PTGS2 were analyzed by combining the clinical data such as staging, histology, survival time and so on. Based on GSEA, the biological functions which were significantly activated in patients with high expression of PTGS2 were identified and the colon cancer cell line SW480 was used as an example for in vitro validation. PTGS2 over-expressing cell strains were constructed, and the effect on cell proliferation was determined by CCK8 method. Different concentrations of H2O2, were used to form gradient oxidative stress, and the changes in cell antioxidant capacity were detected. The regulatory mechanism was preliminarily verified by Western blot. Results The transcription and expression of PTGS2 were found to be significantly up-regulated in colon cancer patients (P<0.05), and the increased expression of PTGS2 was associated with an increased mortality risk (P<0.05). Data analysis and in vitro experiments showed that over-expression of PTGS2 may promote the proliferation of colon cancer cells by activating the mTOR pathway. The antioxidant effect of cells was regulated by up-regulating oxidative stress regulatory proteins SOD2 and NRF2. Conclusions PTGS2 is a potential risk factor for colon cancer and its over-expression promotes cell proliferation, enhances cell antioxidant effect and is associated with poor prognosis of colon cancer patients. [ABSTRACT FROM AUTHOR]

目的基于前列腺素内过氧化物合成酶2 (PTGS2) 在结肠癌中的表达及预后分析,探讨并验证 PTGS2 影响结 肠癌患者预后的潜在分子机制。方法从TCGA、HPA、UALCAN等数据库收集泛癌的转录组和蛋白质组学数据,并 结合肿瘤患者的分期分型、生存时间等临床数据,分析PTGS2 基因的表达模式和预后价值。基于基因集合富集分 析 (GSEA) 鉴定在 PTGS2 高表达患者中显著激活的生物学功能,并以结肠癌细胞系SW480为例,进行体外验证。 构建 PTGS2 过表达细胞株,使用CCK8法测定对细胞增殖的影响;使用不同浓度 H2O2,形成梯度氧化胁迫,检测细 胞抗氧化能力的变化;并通过蛋白质免疫印迹初步验证其调控机制。结果 PTGS2 的转录水平和表达水平在结肠 癌患者中均显著上调 (P<0.05),且PTGS2的表达升高与患者的死亡风险升高相关 (P<0.05) 。数据分析和体外实 验表明过表达 PTGS2可能通过激活 mTOR 通路促进结肠癌细胞增殖;并通过上调氧化应激调控蛋白 SOD2、NRF2 调控细胞抗氧化能力。结论PTGS2是一个潜在的结肠癌危险因素,其表达水平升高促进细胞增殖,增强细胞抗氧 化能力,并与结肠癌患者不良预后相关。 [ABSTRACT FROM AUTHOR]

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