Cargando…
LOC134466 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 LOC134466 was chosen for the further research. We al...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286819/ https://www.ncbi.nlm.nih.gov/pubmed/30485833 http://dx.doi.org/10.18632/aging.101644 |
_version_ | 1783379529682649088 |
---|---|
author | Xu, Hai Sun, Yuan Ma, Zhen Xu, Xin Qin, Lili Luo, Baoping |
author_facet | Xu, Hai Sun, Yuan Ma, Zhen Xu, Xin Qin, Lili Luo, Baoping |
author_sort | Xu, Hai |
collection | PubMed |
description | 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 LOC134466 was chosen for the further research. We also found that TAC1 was the target gene of LOC134466 and miRNA, hsa-miR-196a-5p, might form a connection between LOC134466 and TAC1. The relationship was further proved by dual-luciferase reporter assay. In vitro 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 LOC134466 and TAC1 in EC was further confirmed by Tumor Xenograft. Our results indicated that EC progression was promoted by hypermethylated LOC134466 and TAC1. Moreover, TAC1 transcription was regulated by LOC134466 via hsa-miR-196a-5p binding. LOC134466 and TAC1 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 LOC134466 and TAC1 treatments. Our findings establish a novel regulatory axis, LOC134466/hsa-miR-196a-5p/TAC1. Downregulation of the axis promoted EC development through TACR3, which further activated neuroactive ligand-receptor interaction. |
format | Online Article Text |
id | pubmed-6286819 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-62868192018-12-17 LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis Xu, Hai Sun, Yuan Ma, Zhen Xu, Xin Qin, Lili Luo, Baoping Aging (Albany NY) Research Paper 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 LOC134466 was chosen for the further research. We also found that TAC1 was the target gene of LOC134466 and miRNA, hsa-miR-196a-5p, might form a connection between LOC134466 and TAC1. The relationship was further proved by dual-luciferase reporter assay. In vitro 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 LOC134466 and TAC1 in EC was further confirmed by Tumor Xenograft. Our results indicated that EC progression was promoted by hypermethylated LOC134466 and TAC1. Moreover, TAC1 transcription was regulated by LOC134466 via hsa-miR-196a-5p binding. LOC134466 and TAC1 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 LOC134466 and TAC1 treatments. Our findings establish a novel regulatory axis, LOC134466/hsa-miR-196a-5p/TAC1. Downregulation of the axis promoted EC development through TACR3, which further activated neuroactive ligand-receptor interaction. Impact Journals 2018-11-28 /pmc/articles/PMC6286819/ /pubmed/30485833 http://dx.doi.org/10.18632/aging.101644 Text en Copyright © 2018 Xu et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Xu, Hai Sun, Yuan Ma, Zhen Xu, Xin Qin, Lili Luo, Baoping LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis |
title | LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis |
title_full | LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis |
title_fullStr | LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis |
title_full_unstemmed | LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis |
title_short | LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis |
title_sort | loc134466 methylation promotes oncogenesis of endometrial carcinoma through loc134466/hsa-mir-196a-5p/tac1 axis |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286819/ https://www.ncbi.nlm.nih.gov/pubmed/30485833 http://dx.doi.org/10.18632/aging.101644 |
work_keys_str_mv | AT xuhai loc134466methylationpromotesoncogenesisofendometrialcarcinomathroughloc134466hsamir196a5ptac1axis AT sunyuan loc134466methylationpromotesoncogenesisofendometrialcarcinomathroughloc134466hsamir196a5ptac1axis AT mazhen loc134466methylationpromotesoncogenesisofendometrialcarcinomathroughloc134466hsamir196a5ptac1axis AT xuxin loc134466methylationpromotesoncogenesisofendometrialcarcinomathroughloc134466hsamir196a5ptac1axis AT qinlili loc134466methylationpromotesoncogenesisofendometrialcarcinomathroughloc134466hsamir196a5ptac1axis AT luobaoping loc134466methylationpromotesoncogenesisofendometrialcarcinomathroughloc134466hsamir196a5ptac1axis |