Abstract
ObjectiveTo investigate the mechanism of lncRNA SNHG1 in the immune escape of breast cancer (BC). MethodsSNHG1, miR-448 and IL-10 levels were evaluated by qRT-PCR. The protein levels of IDO and Foxp3 were measured by Western blot. SNHG1 and miR-448 interaction was tested by RIP assay and RNA pull-down assay. MiR-448 and IDO interaction was observed by luciferase reporter assay. ResultsCompared with CD4+T cells, miR-448 expression in CD4+ TIL cells was decreased, while the expression of SNHG1, IDO, IL-10 and Foxp3 were increased. Moreover, SNHG1 directly contacted with miR-448, which could negatively regulate IDO. In cells treated with siRNA-SNHG and miR-448 inhibitor, interference SNHG1 up-regulated miR-448 expression and down-regulated IDO expression, while miR-448 inhibitor reversed this effect. In addition, miR-448 inhibitor reversed the inhibitory effect of siRNA-SNHG1 on Treg cell differentiation, and siRNA-SNHG1 could reduce tumor volume and down-regulated the expressions of SNHG1, IL-10, IDO and Foxp3. ConclusionInterference SNHG1 could inhibit the differentiation of Treg cells by promoting miR-448 expression and reducing IDO level, thereby impeding the immune escape of BC.
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