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Upregulated long noncoding RNA SPRY4-IT1 contributes to increased cell viability by activating zinc finger 703 expression in esophageal squamous cell carcinoma.
Indian Journal of Cancer 2015 December
OBJECTIVES: The function of long noncoding RNA SPRY4-IT1 in human esophageal squamous cell carcinoma (ESCC) has been showed in the former studies. The purpose of this study was to further analyze the underlined mechanisms responsible for its role in ESCC cells.
MATERIALS AND METHODS: Quantitative reverse transcriptase polymerase chain reaction was firstly used to measure the expression of SPRY4-IT1 in 50 ESCC patients of different clinical stages. Loss of function approach was then applied to confirm the biological function, especially cell viabilities in cultured ESCC cells, by cell counting kit-8 and clonogenic assay. We further used western blot to reveal the activation of zinc finger 703 (ZNF703) by SPRY4-IT1.
RESULTS: We validated that SPRY4-IT1 was upregulated in ESCC tissues of advanced clinical stages. In vitro function assays demonstrated that SPRY4-IT1 cause promotion of cell viability in ESCC cells. We further verified that SPRY4-IT1 could also activate the expression of ZNF703 in ESCC cells, which might contribute to the role of SPRY4-IT1 in ESCC cells.
CONCLUSION: SPRY4-IT1 is a vital regulator in ESCC progression, and the SPRY4-IT1/ZNF703 axis might provide novel clues for future ESCC therapy.
MATERIALS AND METHODS: Quantitative reverse transcriptase polymerase chain reaction was firstly used to measure the expression of SPRY4-IT1 in 50 ESCC patients of different clinical stages. Loss of function approach was then applied to confirm the biological function, especially cell viabilities in cultured ESCC cells, by cell counting kit-8 and clonogenic assay. We further used western blot to reveal the activation of zinc finger 703 (ZNF703) by SPRY4-IT1.
RESULTS: We validated that SPRY4-IT1 was upregulated in ESCC tissues of advanced clinical stages. In vitro function assays demonstrated that SPRY4-IT1 cause promotion of cell viability in ESCC cells. We further verified that SPRY4-IT1 could also activate the expression of ZNF703 in ESCC cells, which might contribute to the role of SPRY4-IT1 in ESCC cells.
CONCLUSION: SPRY4-IT1 is a vital regulator in ESCC progression, and the SPRY4-IT1/ZNF703 axis might provide novel clues for future ESCC therapy.
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