Conclusion
MiR143HG may up-regulate p53 in EC by sponging miR-125a to promote cancer cell apoptosis.
Methods
Gene expression was analyzed by qPCR and Western blot. Interactions among genes were analyzed by over-expression experiments. Cell apoptosis after transfections was analyzed by cell apoptosis assay.
Results
We found that the down-regulation of miR143HG in EC predicted poor survival. Bioinformatics analysis showed that miR-125a could bind miR143HG. In EC tissues, miR143HG was positively correlated with p53, not miR-125a. In EC cells, miR143HG and miR-125a over-expression failed to affect the expression of each other. However, miR143HG over-expression led to the up-regulated p53. MiR-125a over-expression played the opposite role and attenuated the effects of miR143HG over-expression. Cell apoptosis analysis showed that miR143HG and p53 over-expression led to an increased cell apoptotic rate. MiR-125a over-expression played the opposite role and attenuated the effects of miR143HG over-expression.