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Aquaporin-1 facilitates proliferation and invasion of gastric cancer cells via GRB7-mediated ERK and Ras activation
Animal Cells and Systems ( IF 2.5 ) Pub Date : 2020-09-02 , DOI: 10.1080/19768354.2020.1833985
Zhenjie Wang 1 , Yujuan Wang 2 , Yuan He 3 , Ning Zhang 1 , Wei Chang 4 , Yahui Niu 1
Affiliation  

ABSTRACT Gastric cancer, one of the most common malignant tumors of the digestive tract, is devoid of effective treatment owing to its highly invasive ability. Aquaporins (AQPs), transmembrane water channel proteins, has been shown to be involved in the malignancy of gastric cancer. This study aims to investigate the pathophysiological roles of AQP-1 in gastric cancer. We first demonstrated quantitative real-time polymerase chain reaction analysis and found up-regulation of AQP-1 in gastric cancer cell lines. Additionally, silence of AQP-1 inhibited cell proliferation via decrease of proliferating cell nuclear antigen (PCNA) and minichromosome maintenance complex component 2 (MCM2). Moreover, migration and invasion of gastric cancer cells were also suppressed by the interference of AQP-1. However, the tumorigenic mechanism of AQP-1 on gastric cancer is yet to be found. We demonstrated western blot analysis and found that knockdown of AQP-1 decreased protein expression of phospho (p)-GRB7 (growth factor receptor-bound protein 7) and led to a remarkable reduction of p-extracellular signal-regulated kinase (ERK) via inactivation of RAS. In general, our findings indicated that AQP-1 facilitates proliferation and invasion of gastric cancer cells via GRB7-mediated ERK and Ras activation, illuminating a novel AQP-1-RAS/ERK molecular axis as regulator in gastric cancer progression and suggesting potential implications in the treatment of gastric cancer.

中文翻译:

Aquaporin-1通过GRB7介导的ERK和Ras激活促进胃癌细胞的增殖和侵袭

摘要 胃癌是消化道最常见的恶性肿瘤之一,由于其侵袭性强,缺乏有效的治疗方法。水通道蛋白 (AQPs) 是一种跨膜水通道蛋白,已被证明与胃癌的恶性肿瘤有关。本研究旨在探讨 AQP-1 在胃癌中的病理生理作用。我们首先展示了定量实时聚合酶链反应分析,并发现了胃癌细胞系中 AQP-1 的上调。此外,AQP-1 的沉默通过减少增殖细胞核抗原 (PCNA) 和微染色体维持复合物组分 2 (MCM2) 来抑制细胞增殖。此外,AQP-1的干扰也抑制了胃癌细胞的迁移和侵袭。然而,AQP-1对胃癌的致瘤机制尚未发现。我们展示了蛋白质印迹分析,发现 AQP-1 的敲低降低了磷酸化 (p)-GRB7(生长因子受体结合蛋白 7)的蛋白表达,并导致 p-细胞外信号调节激酶 (ERK) 通过RAS 失活。总的来说,我们的研究结果表明,AQP-1 通过 GRB7 介导的 ERK 和 Ras 激活促进胃癌细胞的增殖和侵袭,阐明了一种新的 AQP-1-RAS/ERK 分子轴作为胃癌进展的调节剂,并暗示了其潜在的影响。胃癌的治疗。我们展示了蛋白质印迹分析,发现 AQP-1 的敲低降低了磷酸化 (p)-GRB7(生长因子受体结合蛋白 7)的蛋白表达,并导致 p-细胞外信号调节激酶 (ERK) 通过RAS 失活。总的来说,我们的研究结果表明,AQP-1 通过 GRB7 介导的 ERK 和 Ras 激活促进胃癌细胞的增殖和侵袭,阐明了一种新的 AQP-1-RAS/ERK 分子轴作为胃癌进展的调节剂,并暗示了其潜在的影响。胃癌的治疗。我们展示了蛋白质印迹分析,发现 AQP-1 的敲低降低了磷酸化 (p)-GRB7(生长因子受体结合蛋白 7)的蛋白表达,并导致 p-细胞外信号调节激酶 (ERK) 通过RAS 失活。总的来说,我们的研究结果表明,AQP-1 通过 GRB7 介导的 ERK 和 Ras 激活促进胃癌细胞的增殖和侵袭,阐明了一种新的 AQP-1-RAS/ERK 分子轴作为胃癌进展的调节剂,并暗示了其潜在的影响。胃癌的治疗。
更新日期:2020-09-02
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