Abstract
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.
Highlights
Gastric cancer (GC) ranks third in the tumor mortality rate over the world [1]
Threonine aspartase 1 (TASP1) is not a traditional oncogene, but it can help the occurrence of cancer by cleaving mixed lineage leukemia 1 (MLL) and TFIIA and be a potential anticancer drug target [13, 24]
It is the first time to report that the levels of TASP1 in GC patients tissues and GC cells are significantly upregulated
Summary
Gastric cancer (GC) ranks third in the tumor mortality rate over the world [1]. Most GC patients have no obvious symptoms in the early stage and are diagnosed at an advanced stage due to the deficiency of clinically effective markers [2]. The sensitivity and specificity of these biomarkers are still low [3]. Recent studies reported several novel biomarkers such as pepsinogen, α-fetoprotein, M2-pyruvate kinase, vascular adhesion protein-1, microRNA, long noncoding RNA, and circular. In the treatment of gastric cancer, apart from minimally invasive gastrectomy and radiotherapy, chemotherapy drugs are approved for the clinical treatment of GC patients, whose survival rate is low yet [5,6,7,8,9,10]. There is still an urgent need to discover new biomarkers and therapeutic targets
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