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TASP1 Promotes Proliferation and Migration in Gastric Cancer via EMT and AKT/P-AKT Pathway

机译:TASP1通过EMT和AKT / P-AKT途径促进胃癌中的增殖和迁移

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Threonine aspartase 1 (TASP1) was reported to function in the development of cancer. However, the regulatory mechanism of TASP1 in gastric cancer (GC) remains unclear. In this study, we determined the expression of TASP1 in tissues of GC patients, GC cells by qRT-PCR, and western blot and assessed the relationship between TASP1 and GC cell proliferation and migration via CCK-8 and transwell assay. It was found that the expression of TASP1 in GC tissues or GC cell lines was significantly higher than that in normal adjacent tissues or normal cells. The proliferation and migration of GC cells were inhibited upon TASP1 knockdown. Mechanism investigation revealed that TASP1 promoted GC cell proliferation and migration through upregulating the p-AKT/AKT expression. TASP1 induced GC cell migration via the epithelial -mesenchymal transition (EMT) pathway. In conclusion, TASP1 promotes GC progression through the EMT and AKT/p-AKT pathway, and it may serve as a new potential biomarker and therapeutic target for GC.
机译:据报道,苏氨酸aspartase1(Task1)在癌症的发展中起作用。然而,胃癌中TASP1(GC)的调节机制仍不清楚。在这项研究中,我们确定了通过QRT-PCR的GC患者,GC细胞组织中TAP1的表达,并评估了TASP1和GC细胞增殖与通过CCK-8和Transwell测定的迁移之间的关系。发现GC组织或GC细胞系中TASP1的表达明显高于正常相邻组织或正常细胞中的TAP1。在TASP1敲低时抑制了GC细胞的增殖和迁移。机制调查显示,TASP1通过上调P-AKT / AKT表达来促进GC细胞增殖和迁移。 TASP1通过上皮 - 发育过渡(EMT)途径诱导GC细胞迁移。总之,TASP1通过EMT和AKT / P-AKT途径促进GC进展,它可以作为GC的新潜在的生物标志物和治疗靶标。

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