PMID- 27698829
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 12
IP  - 4
DP  - 2016 Oct
TI  - MicroRNA-486-5p enhances hepatocellular carcinoma tumor suppression through 
      repression of IGF-1R and its downstream mTOR, STAT3 and c-Myc.
PG  - 2567-2573
AB  - The insulin-like growth factor (IGF)-axis has been paradigmatically involved in 
      hepatocellular carcinoma (HCC) tumor initiation, progression and drug resistance. 
      Consequently, members of the IGF-axis and most importantly, IGF-1 receptor 
      (IGF-1R) have been considered as intriguing targets for HCC therapy. Few miRNAs 
      have been recently reported to be associated with IGF-1R regulation. The present 
      study aimed to investigate the role of microRNA (miRNA/miR)-486-5p in the 
      regulation of IGF-1R and its downstream signaling cascades. miR-486-5p was 
      markedly downregulated in hepatitis C virus-induced HCC tissues and Huh-7 cells. 
      Forcing the expression of miR-486-5p in Huh-7 cells resulted in the repression of 
      IGF-1R, mammalian target of rapamycin (mTOR), signal transducer and activator of 
      transcription 3 (STAT3) and c-Myc mRNA levels. Ectopic expression of miR-486-5p 
      in Huh-7 cells markedly repressed cellular viability, proliferation, migration 
      and clonogenicity in a similar pattern to IGF-1R small interfering RNAs, and were 
      evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, 
      BrdU incorporation, wound healing and colony forming assays, respectively. 
      Overall, the study findings demonstrated that miR-486-5p acts as a tumor 
      suppressor in HCC through the repression of essential members of the IGF-axis, 
      including IGF-1R and its downstream mediators mTOR, STAT3 and c-Myc.
FAU - Youness, Rana Ahmed
AU  - Youness RA
AD  - Department of Pharmaceutical Biology, Faculty of Pharmacy and Biotechnology, 
      German University in Cairo, New Cairo City, Cairo 11835, Egypt.
FAU - El-Tayebi, Hend Mohamed
AU  - El-Tayebi HM
AD  - Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, 
      German University in Cairo, New Cairo City, Cairo 11835, Egypt.
FAU - Assal, Reem Amr
AU  - Assal RA
AD  - Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, 
      German University in Cairo, New Cairo City, Cairo 11835, Egypt.
FAU - Hosny, Karim
AU  - Hosny K
AD  - Department of General Surgery, Faculty of Medicine, Cairo University, Giza 12613, 
      Egypt.
FAU - Esmat, Gamal
AU  - Esmat G
AD  - Department of Endemic Medicine and Hepatology, Cairo University, Giza 12613, 
      Egypt.
FAU - Abdelaziz, Ahmed Ihab
AU  - Abdelaziz AI
AD  - Department of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, 
      German University in Cairo, New Cairo City, Cairo 11835, Egypt.
LA  - eng
PT  - Journal Article
DEP - 20160727
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC5038225
OTO - NOTNLM
OT  - HCC
OT  - IGF-1R
OT  - STAT3
OT  - c-Myc
OT  - mTOR
OT  - microRNA-486-5p
EDAT- 2016/10/05 06:00
MHDA- 2016/10/05 06:01
PMCR- 2016/07/27
CRDT- 2016/10/05 06:00
PHST- 2015/08/03 00:00 [received]
PHST- 2016/06/16 00:00 [accepted]
PHST- 2016/10/05 06:00 [entrez]
PHST- 2016/10/05 06:00 [pubmed]
PHST- 2016/10/05 06:01 [medline]
PHST- 2016/07/27 00:00 [pmc-release]
AID - OL-0-0-4914 [pii]
AID - 10.3892/ol.2016.4914 [doi]
PST - ppublish
SO  - Oncol Lett. 2016 Oct;12(4):2567-2573. doi: 10.3892/ol.2016.4914. Epub 2016 Jul 
      27.