methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis.

To investigate possible mechanism of abnormal methylation of long non-coding RNA (lncRNA) on endometrial carcinoma (EC) progression, we detected the genome methylation profiling of endometrial carcinoma by bioinformatic analysis. Accordingly, gene was chosen for the further research. We also found that was the target gene of and miRNA, hsa-miR-196a-5p, might form a connection between and . The relationship was further proved by dual-luciferase reporter assay. studies, DNA methylation and expression were determined by MSP and qRT-PCR respectively. Cell proliferation, apoptosis and cell cycle were demonstrated by colony formation assay, Annexin V/PI double staining and flow cytometry. Besides, the function of and in EC was further confirmed by Tumor Xenograft. Our results indicated that EC progression was promoted by hypermethylated and . Moreover, transcription was regulated by via hsa-miR-196a-5p binding. and demethylation by 5-Aza-2-Deoxycytidine inhibited EC cells proliferation and accelerated cell apoptosis. Furthermore, the expression of TACR1, TACR2 and TACR3 was remarkably decreased through and treatments. Our findings establish a novel regulatory axis, /hsa-miR-196a-5p/ Downregulation of the axis promoted EC development through TACR3, which further activated neuroactive ligand-receptor interaction.