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Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression
Gastroenterology Research and Practice ( IF 2.0 ) Pub Date : 2021-08-05 , DOI: 10.1155/2021/5527387
Jun Wang 1 , Zhigang He 2 , Bo Sun 3 , Wenhai Huang 1 , Jianbin Xiang 1 , Zongyou Chen 1 , Zhenyang Li 1 , Xiaodong Gu 1
Affiliation  

Pleckstrin-2 (PLEK2) is a crucial mediator of cytoskeletal reorganization. However, the potential roles of PLEK2 in gastric cancer are still unknown. PLEK2 expression in gastric cancer was examined by western blotting and real-time PCR. Survival analysis was utilized to test the clinical impacts of the levels of PLEK2 in gastric cancer patients. In vitro and in vivo studies were used to estimate the potential roles played by PLEK2 in modulating gastric cancer proliferation, self-renewal, and tumourigenicity. Bioinformatics approaches were used to monitor the effect of PLEK2 on epithelial-mesenchymal transition (EMT) signalling pathways. PLEK2 expression was significantly upregulated in gastric cancer as compared with nontumour samples. Kaplan-Meier plotter analysis revealed that gastric cancer patients with higher PLEK2 levels had substantially poorer overall survival compared with gastric cancer patients with lower PLEK2 levels. The upregulation or downregulation of PLEK2 in gastric cancer cell lines effectively enhanced or inhibited cell proliferation and proinvasive behaviour, respectively. Additionally, we also found that PLEK2 enhanced EMT through downregulating E-cadherin expression and upregulating Vimentin expression. Our findings demonstrated that PLEK2 plays a potential role in gastric cancer and may be a novel therapeutic target for gastric cancer.

中文翻译:

Pleckstrin-2 作为胃癌进展的预后因素和介质

Pleckstrin-2 (PLEK2) 是细胞骨架重组的关键介质。然而,PLEK2在胃癌中的潜在作用仍然未知。通过蛋白质印迹和实时PCR检测胃癌中PLEK2的表达。生存分析用于测试 PLEK2 水平对胃癌患者的临床影响。体外和体内研究用于评估 PLEK2 在调节胃癌增殖、自我更新和致瘤性方面的潜在作用。生物信息学方法用于监测 PLEK2 对上皮间质转化 (EMT) 信号通路的影响。与非肿瘤样本相比,PLEK2 表达在胃癌中显着上调。Kaplan-Meier 绘图仪分析显示,与 PLEK2 水平较低的胃癌患者相比,PLEK2 水平较高的胃癌患者的总体生存率显着降低。胃癌细胞系中PLEK2的上调或下调分别有效地增强或抑制了细胞增殖和促侵袭行为。此外,我们还发现 PLEK2 通过下调 E-cadherin 表达和上调波形蛋白表达来增强 EMT。我们的研究结果表明,PLEK2 在胃癌中发挥潜在作用,可能是胃癌的新治疗靶点。胃癌细胞系中PLEK2的上调或下调分别有效地增强或抑制了细胞增殖和促侵袭行为。此外,我们还发现 PLEK2 通过下调 E-cadherin 表达和上调波形蛋白表达来增强 EMT。我们的研究结果表明,PLEK2 在胃癌中发挥潜在作用,可能是胃癌的新治疗靶点。胃癌细胞系中PLEK2的上调或下调分别有效地增强或抑制了细胞增殖和促侵袭行为。此外,我们还发现 PLEK2 通过下调 E-cadherin 表达和上调波形蛋白表达来增强 EMT。我们的研究结果表明,PLEK2 在胃癌中发挥潜在作用,可能是胃癌的新治疗靶点。
更新日期:2021-08-05
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