PMID- 29059496
OWN - NLM
STAT- MEDLINE
DCOM- 20180123
LR  - 20211204
IS  - 1349-7006 (Electronic)
IS  - 1347-9032 (Print)
IS  - 1347-9032 (Linking)
VI  - 109
IP  - 1
DP  - 2018 Jan
TI  - Increased T-helper 17 cell differentiation mediated by exosome-mediated 
      microRNA-451 redistribution in gastric cancer infiltrated T cells.
PG  - 65-73
LID - 10.1111/cas.13429 [doi]
AB  - MicroRNA (miR)-451 is a cell metabolism-related miRNA that can mediate cell 
      energy-consuming models by several targets. As miR-451 can promote mechanistic 
      target of rapamycin (mTOR) activity, and increased mTOR activity is related to 
      increased differentiation of T-helper 17 (Th17) cells, we sought to investigate 
      whether miR-451 can redistribute from cancer cells to infiltrated T cells and 
      enhance the distribution of Th17 cells through mTOR. Real-time PCR was used for 
      detecting expression of miR-451 in gastric cancer, tumor infiltrated T cells and 
      exosomes, and distribution of Th17 was evaluated by both flow cytometry and 
      immunohistochemistry (IHC). Immunofluorescence staining was used in monitoring 
      the exosome-enveloped miR-451 from cancer cells to T cells with different 
      treatments, and signaling pathway change was analyzed by western blot. miR-451 
      decreased significantly in gastric cancer (GC) tissues but increased in 
      infiltrated T cells and exosomes; tumor miR-451 was negatively related to 
      infiltrated T cells and exosome miR-451. Exosome miR-451 can not only serve as an 
      indicator for poor prognosis of post-operation GC patients but is also related to 
      increased Th17 distribution in gastric cancer. miR-451 can redistribute from 
      cancer cells to T cells with low glucose treatment. Decreased 5' AMP-activated 
      protein kinase (AMPK) and increased mTOR activity was investigated in miR-451 
      redistributed T cells and the Th17 polarized differentiation of these T cells 
      were also increased. Exosome miR-451 derived from tumor tissues can serve as an 
      indicator for poor prognosis and redistribution of miR-451 from cancer cells to 
      infiltrated T cells in low glucose treatment can enhance Th17 differentiation by 
      enhancing mTOR activity.
CI  - (c) 2017 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd 
      on behalf of Japanese Cancer Association.
FAU - Liu, Feng
AU  - Liu F
AD  - Department of ICU, the 359th Hospital of PLA, Zhenjiang, China.
FAU - Bu, Zhouyan
AU  - Bu Z
AD  - Changzhou Zhengheng Middle School, Changzhou, China.
FAU - Zhao, Feng
AU  - Zhao F
AD  - Department of Ultrasonography, Hospital Affiliated to Jiangsu University, 
      Zhenjiang, China.
FAU - Xiao, Daping
AU  - Xiao D
AUID- ORCID: 0000-0003-4422-6389
AD  - Department of Clinical Laboratory, the 359th Hospital of PLA, Zhenjiang, China.
LA  - eng
PT  - Journal Article
DEP - 20171110
PL  - England
TA  - Cancer Sci
JT  - Cancer science
JID - 101168776
RN  - 0 (MIRN451 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Cell Differentiation
MH  - Cell Line, Tumor
MH  - Cell Polarity
MH  - Exosomes/*genetics
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Lymphocyte Activation
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Neoplasm Staging
MH  - Prognosis
MH  - Signal Transduction
MH  - Stomach Neoplasms/*genetics/metabolism/pathology/*surgery
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Th17 Cells/chemistry/*cytology
PMC - PMC5765284
OTO - NOTNLM
OT  - Th17
OT  - exosome
OT  - gastric cancer
OT  - mTOR
OT  - miR-451
EDAT- 2017/10/24 06:00
MHDA- 2018/01/24 06:00
PMCR- 2018/01/01
CRDT- 2017/10/24 06:00
PHST- 2017/07/24 00:00 [received]
PHST- 2017/10/14 00:00 [revised]
PHST- 2017/10/18 00:00 [accepted]
PHST- 2017/10/24 06:00 [pubmed]
PHST- 2018/01/24 06:00 [medline]
PHST- 2017/10/24 06:00 [entrez]
PHST- 2018/01/01 00:00 [pmc-release]
AID - CAS13429 [pii]
AID - 10.1111/cas.13429 [doi]
PST - ppublish
SO  - Cancer Sci. 2018 Jan;109(1):65-73. doi: 10.1111/cas.13429. Epub 2017 Nov 10.