201. Tensin4 promotes invasion and migration of gastric cancer cells via regulating AKT/GSK-3β/snail signaling pathway.
- Author
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Qi X, Sun L, Wan J, Xu R, He S, and Zhu X
- Subjects
- Aged, Cell Movement physiology, Female, Gene Expression Regulation, Neoplastic physiology, Glycogen Synthase Kinase 3 beta metabolism, Humans, Male, Middle Aged, Neoplasm Invasiveness pathology, Proto-Oncogene Proteins c-akt metabolism, Snail Family Transcription Factors metabolism, Adenocarcinoma pathology, Biomarkers, Tumor analysis, Signal Transduction physiology, Stomach Neoplasms pathology, Tensins metabolism
- Abstract
Gastric cancer (GC) remains one of the most lethal human malignancies, and exploring novel therapeutic targets for the treatment has been a major focus. The molecular mechanism of invasion and migration of GC cells remains unclear. The present study aimed to investigate the role of Tensin 4 and the associated molecular signaling pathways in the process of invasion and metastasis of GC. The expression of Tensin 4 protein and phosphorylated AKT (p-AKT) were evaluated in GC and normal adjacent tissues of 80 patients using immunohistochemistry staining. The expression of Tensin4 mRNA was analyzed in 10 GC tissues and 3 GC cell lines (SGC7901, MKN45, and MKN28) by qPCR. Cell proliferation, migration, and invasion were assessed using CCK-8 and Transwell assays in the Tensin 4 siRNA transfected SGC7901 cells and Tensin 4 plasmid transfected MKN28 cells. Additionally, protein expressions of Tensin 4, E-cadherin, vimentin, AKT, p-AKT, GSK-3β, p-GSK-3β, and Snail were analyzed by western blotting. The results demonstrated that the expression of Tensin 4 was significantly up-regulated in the GC tissues and cell lines, especially in the SGC7901 cells. The expression of Tensin 4 positively correlated with p-AKT in GC tissues and with GC progression, and was an independent risk factor for the prognosis of GC. Tensin 4 promoted the invasion and migration abilities of GC cells, but had no significant effect on GC cell proliferation. Tensin 4 promoted the occurrence of epithelial mesenchymal transition (EMT) through up-regulating the expression of p-AKT, p-GSK-3β, and snail. Overall, this study suggests that the activation of AKT/GSK-3β/Snail signaling pathway promoted by Tensin 4 plays an important role in the progression of GC. Therefore, Tensin 4 may serve as a potential target in GC treatment., Competing Interests: Declaration of Competing Interest The authors declared that they have no conflicts of interest to this work. We declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted., (Copyright © 2020 Elsevier GmbH. All rights reserved.)
- Published
- 2020
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