PMID- 32803763 OWN - NLM STAT- MEDLINE DCOM- 20210830 LR - 20211204 IS - 1097-4652 (Electronic) IS - 0021-9541 (Linking) VI - 236 IP - 1 DP - 2021 Jan TI - Long noncoding RNA NEAT1 promotes progression of glioma as a ceRNA by sponging miR-185-5p to stimulate DNMT1/mTOR signaling. PG - 121-130 LID - 10.1002/jcp.29644 [doi] AB - Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) is regarded as an oncogene in multiple cancers. Previous studies have shown that NEAT1 is involved in the proliferation and tumorigenesis of glioma cells, while miR-185-5p functions as a tumor suppressor in glioma. However, the underlying molecular mechanism of NEAT1 in glioma, especially in association with miR-185-5p, has not been studied. In this study, we first demonstrated that NEAT1 expression was upregulated, and miR-185-5p downregulated in glioma tissues and cells. More important, NEAT1 expression was negatively correlated with miR-185-5p expression in glioma tissues. In vitro and in vivo experiments verified that NEAT1 was a competing endogenous RNA for miR-185-5p for promoting DNA methyltransferase 1 (DNMT1) expression and activated mammalian target of rapamycin (mTOR) signaling, thus inhibiting apoptosis, and promoting glioma migration, proliferation, and epithelial-mesenchymal transition process. Furthermore, NEAT1 knockdown suppressed tumor growth and reduced the expression of proliferation antigen Ki-67, DNMT1, and mTOR, but upregulated the expression of miR-185-5p in vivo. Finally, with mTOR inhibitor rapamycin, we confirmed that NEAT1 promoted glioma activity through mTOR signaling both in vitro and in vivo. In conclusion, these results suggest that NEAT1 promotes glioma tumorigenesis via miR-185-5p/DNMT1/mTOR signaling, which may provide a new target for the diagnosis and therapy of glioma. CI - (c) 2020 Wiley Periodicals, Inc. FAU - Yu, Heng AU - Yu H AD - Department of Clinical Laboratory, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China. FAU - Xu, Anchun AU - Xu A AD - Department of Clinical Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China. FAU - Wu, Bo AU - Wu B AD - Department of Clinical Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China. FAU - Wang, Meng AU - Wang M AUID- ORCID: 0000-0002-5909-6014 AD - Department of Rehabilitation, Huai'an Second People's Hospital, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, China. FAU - Chen, Zhongjun AU - Chen Z AUID- ORCID: 0000-0003-4148-1683 AD - Department of Neurosurgery, Huai'an Second People's Hospital, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, China. LA - eng PT - Journal Article DEP - 20200816 PL - United States TA - J Cell Physiol JT - Journal of cellular physiology JID - 0050222 RN - 0 (MIRN185 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (NEAT1 long non-coding RNA, human) RN - 0 (RNA, Long Noncoding) RN - EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1) RN - EC 2.1.1.37 (DNMT1 protein, human) RN - EC 2.7.1.1 (MTOR protein, human) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) SB - IM MH - Apoptosis/genetics MH - Cell Line, Tumor MH - Cell Movement/genetics MH - Cell Proliferation/genetics MH - Cell Transformation, Neoplastic/genetics/pathology MH - DNA (Cytosine-5-)-Methyltransferase 1/*genetics MH - Disease Progression MH - Down-Regulation/genetics MH - Epithelial-Mesenchymal Transition/genetics MH - Gene Expression Regulation, Neoplastic/genetics MH - Glioma/*genetics/pathology MH - Humans MH - MicroRNAs/*genetics MH - RNA, Long Noncoding/*genetics MH - Signal Transduction/*genetics MH - TOR Serine-Threonine Kinases/*genetics MH - Up-Regulation/genetics OTO - NOTNLM OT - DNMT1 OT - NEAT1 OT - ceRNA OT - glioma OT - miR-185-5p EDAT- 2020/08/18 06:00 MHDA- 2021/08/31 06:00 CRDT- 2020/08/18 06:00 PHST- 2019/07/03 00:00 [received] PHST- 2020/02/04 00:00 [accepted] PHST- 2020/08/18 06:00 [pubmed] PHST- 2021/08/31 06:00 [medline] PHST- 2020/08/18 06:00 [entrez] AID - 10.1002/jcp.29644 [doi] PST - ppublish SO - J Cell Physiol. 2021 Jan;236(1):121-130. doi: 10.1002/jcp.29644. Epub 2020 Aug 16.