PMID- 31423233
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 18
IP  - 2
DP  - 2019 Aug
TI  - miR-496, miR-1185, miR-654, miR-3183 and miR-495 are downregulated in colorectal 
      cancer cells and have putative roles in the mTOR pathway.
PG  - 1657-1668
LID - 10.3892/ol.2019.10508 [doi]
AB  - MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression by 
      suppressing the target mRNA and inhibiting translation in order to regulate 
      multiple biological processes. miRNAs play important roles as oncogenes or tumor 
      suppressors in the development of various types of human cancer. The regulation 
      of mammalian target of rapamycin (mTOR) by miRNAs has been studied in several 
      types of cancer, including colorectal cancer (CRC). However, to the best of our 
      knowledge, only limited information regarding the function of miRNAs in human CRC 
      is available. In the present study, the expression of 22 miRNAs in CRC cell lines 
      were investigated in regard to key genes in the mTOR pathway. Initially, it was 
      revealed that mTOR, regulatory-associated protein of mTOR complex I and 
      rapamycin-intensive companion of mTOR were overexpressed in CRC cell lines when 
      compared with a normal colorectal cell line. Subsequently, putative miRNA-mRNA 
      associations were identified via multiple miRNA target prediction programs. The 
      expression levels for the candidate miRNAs were validated using quantitative 
      real-time polymerase chain reaction. Expression analysis revealed that, among 20 
      miRNAs, five miRNAs (miR-496, miR-1185, miR-654, miR-3183 and miR-495) exhibited 
      significant downregulation in association with the mTOR signaling pathway. Taken 
      together, the results from the present study suggest that several miRNAs that are 
      associated with CRC, with possible roles in mTOR signaling, may have potential 
      therapeutic or diagnostic benefits in CRC treatment.
FAU - Alqurashi, Naif
AU  - Alqurashi N
AD  - Department of Basic Science, Deanship of Preparatory Year and Supporting Studies, 
      and Department of Stem Cells, Institute for Research and Medical Consultations, 
      Imam Abdulrahman Bin Faisal University, Dammam 34212, Saudi Arabia.
FAU - Hashimi, Saeed M
AU  - Hashimi SM
AD  - Department of Basic Science, Deanship of Preparatory Year and Supporting Studies, 
      and Department of Stem Cells, Institute for Research and Medical Consultations, 
      Imam Abdulrahman Bin Faisal University, Dammam 34212, Saudi Arabia.
FAU - Alowaidi, Faisal
AU  - Alowaidi F
AD  - Department of Pathology and Laboratory Medicine, College of Medicine and 
      University Hospitals, King Saud University, Riyadh 11451, Saudi Arabia.
FAU - Ivanovski, Saso
AU  - Ivanovski S
AD  - School of Dentistry, The University of Queensland, Brisbane, QLD 4006, Australia.
FAU - Farag, Amro
AU  - Farag A
AD  - School of Dentistry, The University of Queensland, Brisbane, QLD 4006, Australia.
FAU - Wei, Ming Q
AU  - Wei MQ
AD  - Division of Molecular and Gene Therapies, School of Medical Science, Griffith 
      University, Gold Coast, QLD 4222, Australia.
LA  - eng
PT  - Journal Article
DEP - 20190621
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC6614670
OTO - NOTNLM
OT  - colorectal cancer
OT  - mammalian target of rapamycin
OT  - microRNA
OT  - rapamycin-insensitive companion of mammalian target of rapamycin
OT  - regulatory-associated protein of mammalian target of rapamycin complex 1
EDAT- 2019/08/20 06:00
MHDA- 2019/08/20 06:01
PMCR- 2019/06/21
CRDT- 2019/08/20 06:00
PHST- 2019/01/16 00:00 [received]
PHST- 2019/05/02 00:00 [accepted]
PHST- 2019/08/20 06:00 [entrez]
PHST- 2019/08/20 06:00 [pubmed]
PHST- 2019/08/20 06:01 [medline]
PHST- 2019/06/21 00:00 [pmc-release]
AID - OL-0-0-10508 [pii]
AID - 10.3892/ol.2019.10508 [doi]
PST - ppublish
SO  - Oncol Lett. 2019 Aug;18(2):1657-1668. doi: 10.3892/ol.2019.10508. Epub 2019 Jun 
      21.