PMID- 33661803
OWN - NLM
STAT- MEDLINE
DCOM- 20211206
LR  - 20211214
IS  - 1473-558X (Electronic)
IS  - 0959-4965 (Linking)
VI  - 32
IP  - 5
DP  - 2021 Mar 24
TI  - Long noncoding RNA H19 contributes to the proliferation and autophagy of glioma 
      cells through mTOR/ULK1 pathway.
PG  - 352-358
LID - 10.1097/WNR.0000000000001602 [doi]
AB  - Long noncoding RNA (LncRNA) H19 has been proven to be involved in many kinds of 
      cancers including glioma, and a previous study has shown an autophagy regulation 
      of H19. The mammalian target of rapamycin (mTOR) signaling pathway plays a key 
      role in autophagy and Unc-51 like autophagy activating kinase 1 (ULK1) is also 
      thought to be involved in autophagy signaling. In our study, we investigated the 
      role of mTOR/ULK1 autophagy signaling in the H19-mediated promotion of glioma 
      proliferation. Human glioma cells U87 and U251 and normal human astrocytes HA1800 
      were used in the study. First, the expression of H19 was determined in U87, U251, 
      and HA1800 cells. Then, the cell proliferation and migration of glioma cells were 
      detected, while the protein levels of main molecules of the mTOR/ULK1 pathway and 
      autophagy-related proteins were also examined. Rapamycin, an inhibitor of mTOR, 
      was used to further study the role of H19 in autophagy. We observed that 
      overexpressed H19 promoted the proliferation and migration in glioma cells. The 
      autophagy of U87 cells was suppressed when H19 was overexpressed and enhanced 
      when H19 was silenced. H19 overexpression inhibited mTOR phosphorylation and 
      promoted ULK1 phosphorylation. H19 promoted proliferation, migration, and 
      autophagy by regulating mTOR signaling. In conclusion, we validate that H19 
      contributes to the proliferation and autophagy of glioma cells through the 
      mTOR/ULK1 pathway.
CI  - Copyright (c) 2021 Wolters Kluwer Health, Inc. All rights reserved.
FAU - Zhao, Wei
AU  - Zhao W
AD  - Department of Pediatrics, Hangzhou Children's Hospital.
FAU - Lin, Xiaoyan
AU  - Lin X
AD  - Department of Pediatrics.
FAU - Han, Han
AU  - Han H
AD  - Department of Pediatrics.
FAU - Zhang, Hongxu
AU  - Zhang H
AD  - Department of Ophthalmology, Affiliated Hangzhou First People's Hospital, 
      Zhejiang University School of Medicine, Hangzhou First People's Hospital, 
      Hangzhou, Zhejiang, P.R. China.
FAU - Li, Xiaoli
AU  - Li X
AD  - Department of Pediatrics.
FAU - Jiang, Chunming
AU  - Jiang C
AD  - Department of Pediatrics.
FAU - Feng, Mei
AU  - Feng M
AD  - Department of Pediatrics.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Neuroreport
JT  - Neuroreport
JID - 9100935
RN  - 0 (H19 long non-coding RNA)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (RNA, Long Noncoding)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Autophagy-Related Protein-1 Homolog)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (ULK1 protein, human)
SB  - IM
MH  - Autophagy/physiology
MH  - Autophagy-Related Protein-1 Homolog/*metabolism
MH  - Brain Neoplasms/*pathology
MH  - Cell Line, Tumor
MH  - Cell Proliferation/physiology
MH  - Gene Expression Regulation, Neoplastic/physiology
MH  - Glioma/*pathology
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/*metabolism
MH  - RNA, Long Noncoding/*metabolism
MH  - Signal Transduction/physiology
MH  - TOR Serine-Threonine Kinases/*metabolism
EDAT- 2021/03/05 06:00
MHDA- 2021/12/15 06:00
CRDT- 2021/03/04 17:12
PHST- 2021/03/04 17:12 [entrez]
PHST- 2021/03/05 06:00 [pubmed]
PHST- 2021/12/15 06:00 [medline]
AID - 00001756-202103020-00003 [pii]
AID - 10.1097/WNR.0000000000001602 [doi]
PST - ppublish
SO  - Neuroreport. 2021 Mar 24;32(5):352-358. doi: 10.1097/WNR.0000000000001602.