PMID- 30569129
OWN - NLM
STAT- MEDLINE
DCOM- 20190524
LR  - 20211204
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 19
IP  - 3
DP  - 2019 Mar
TI  - MicroRNA‑206 exerts anti‑oncogenic functions in esophageal squamous cell 
      carcinoma by suppressing the c‑Met/AKT/mTOR pathway.
PG  - 1491-1500
LID - 10.3892/mmr.2018.9775 [doi]
AB  - Increasing evidence suggests that the dysregulation of microRNAs (miRNAs) has an 
      important role in the progression of human cancer, including ESCC. However, the 
      exact functions and mechanisms of miRNAs in ESCC remain largely unclear. The aim 
      of the present study was to investigate the expression and biological functions 
      of miRNAs in ESCC and reveal the underlying molecular mechanisms. miRNA 
      microarray and reverse transcription‑quantitative polymerase chain reaction 
      analyses were performed, which identified and confirmed that miR‑206 was 
      significantly downregulated in ESCC tissues and cell lines. Its low expression 
      was associated with lymph node metastasis, advanced TNM stage and N 
      classification, as well as poorer overall survival in patients with ESCC. CCK‑8 
      and flow cytometry assays demonstrated that ectopic miR‑206 expression inhibited 
      ESCC cell proliferation and induced cell apoptosis. In addition, MET 
      proto‑oncogene, receptor tyrosine kinase (c‑Met), a well‑known oncogene, was a 
      direct target of miR‑206. An inverse correlation between the levels of miR‑206 
      and c‑Met mRNA in ESCC tissue samples was confirmed. Notably, c‑Met 
      overexpression inhibited the effects of miR‑206 on the proliferation and 
      apoptosis of ESCC cells. Additionally, it was confirmed that the 
      tumor‑suppressive functions of miR‑206 may have contributed to the inactivation 
      of the c‑Met/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) 
      signaling pathway. In conclusion, the findings of the present study suggested 
      that miR‑206 exerts its anti‑cancer functions via the c‑Met/AKT/mTOR signaling 
      pathway, providing a novel candidate prognostic factor and a potential 
      therapeutic target in ESCC.
FAU - Zhang, Jin
AU  - Zhang J
AD  - Department of Thoracic Surgery, The Second Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan 450014, P.R. China.
FAU - Fa, Xianen
AU  - Fa X
AD  - Department of Cardiac Surgery, The Second Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan 450014, P.R. China.
FAU - Zhang, Qingyong
AU  - Zhang Q
AD  - Department of Thoracic Surgery, The Second Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan 450014, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20181218
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (MIRN206 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.10.1 (MET protein, human)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Aged
MH  - Apoptosis/genetics
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Esophageal Squamous Cell Carcinoma/*genetics/pathology
MH  - Female
MH  - Gene Expression Regulation, Neoplastic/genetics
MH  - Humans
MH  - Lymphatic Metastasis
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Middle Aged
MH  - Oncogene Protein v-akt/genetics
MH  - Proto-Oncogene Proteins c-met/*genetics
MH  - Signal Transduction/genetics
MH  - TOR Serine-Threonine Kinases/*genetics
PMC - PMC6390054
OTO - NOTNLM
OT  - esophageal squamous cell carcinoma
OT  - microRNA‑206
OT  - c-Met
OT  - AKT/mTOR pathway
EDAT- 2018/12/21 06:00
MHDA- 2019/05/28 06:00
PMCR- 2018/12/18
CRDT- 2018/12/21 06:00
PHST- 2018/01/31 00:00 [received]
PHST- 2018/10/12 00:00 [accepted]
PHST- 2018/12/21 06:00 [pubmed]
PHST- 2019/05/28 06:00 [medline]
PHST- 2018/12/21 06:00 [entrez]
PHST- 2018/12/18 00:00 [pmc-release]
AID - mmr-19-03-1491 [pii]
AID - 10.3892/mmr.2018.9775 [doi]
PST - ppublish
SO  - Mol Med Rep. 2019 Mar;19(3):1491-1500. doi: 10.3892/mmr.2018.9775. Epub 2018 Dec 
      18.