Abstract
Purpose: To investigate the effect of tripartite membrane protein TRIM) 16 gene silencing on human esophageal cancer (KYSE-270) cell proliferation, invasion and metastasis.Methods: Short interfering RNA (siRNA) TRIM 16 silencing fragment was transfected into KYSE-270 cells. Transfection efficiency was determined using real-time quantitative polymerase chain reaction (qRT-PCR). Cell proliferation, invasiveness and migration were measured by 3-(4,5-dimethylthiazol2-yl)- 2,5-diphenyl tetrazolium bromide (MTT) assay, Transwell invasion assay, and scratch test, respectively. Protein expressions of bax and bcl-2 were assayed using Western blotting.Results: The gene expression of TRIM 16 was significantly upregulated in esophageal cancer cells, relative to normal human esophageal cells, but was downregulated after gene silencing. Moreover, the silencing of TRIM 16 gene led to significant reductions in KYSE-270 cell viability, migration and invasiveness, but significantly increased KYSE270 cell apoptosis (p < 0.05). The silencing of TRIM 16 gene also significantly upregulated bax protein expression, while downregulating the expression of bcl-2 protein (p < 0.05).Conclusion: These results suggest that TRIM 16 gene silencing inhibits KYSE-270 cell proliferation, invasion and metastasis, and thus provide a basis for its development as a therapeutic approach for the management of esophageal cancer.
 Keywords: Apoptosis, Cell invasion, Esophageal cancer, Gene silencing, Metastasis
Highlights
Esophageal cancer is the seventh leading cause of cancer deaths worldwide [1]
The mRNA expression of Tripartite motif (TRIM) 16 was significantly higher in esophageal cancer cells than in normal human esophageal cells, and was higher in KYSE-270 cells than in the other three esophageal cancer cell lines (p < 0.05)
Effect of Tripartite membrane protein 16 (TRIM 16) gene silencing on the levels of expression of apoptosis-related proteins in KYSE-270 cells
Summary
Esophageal cancer is the seventh leading cause of cancer deaths worldwide [1]. The incidence of esophageal cancer varies, depending on the regions of the world, from 30 cases to as high as 800 cases per 100 000 persons [2]. The high mortality associated with esophageal cancer is attributed to poor prognosis and late diagnosis [3]. 95 % of the pathology of esophageal cancers worldwide, adenocarcinomas are becoming an increasingly prevalent in the western world [2]. Strategies commonly employed for the management of esophageal cancer include surgery, chemotherapy, radiotherapy and laser therapy [4]. Since the 5-year survival is very low, there is need for novel compounds that can effectively alleviate the disease [5].
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