PMID- 31696477
OWN - NLM
STAT- MEDLINE
DCOM- 20201013
LR  - 20211204
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 20
DP  - 2019 Oct
TI  - MicroRNA-646 inhibits proliferation and cell cycle progression of nasopharyngeal 
      carcinoma cells by targeting mTOR.
PG  - 8905-8912
LID - 19286 [pii]
LID - 10.26355/eurrev_201910_19286 [doi]
AB  - OBJECTIVE: To clarify whether microRNA-646 could regulate the proliferative 
      potential and cell cycle progression of nasopharyngeal carcinoma cells through 
      targeting mammalian target of rapamycin (mTOR). It, therefore, could influence 
      the occurrence and progression of nasopharyngeal carcinoma. PATIENTS AND METHODS: 
      Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect 
      expression of the levels of microRNA-646 and mTOR in tumor tissues and 
      paracancerous tissues of patients with nasopharyngeal carcinoma. Besides, their 
      expressions in nasopharyngeal carcinoma cell lines were determined by qRT-PCR. 
      Survival analysis was conducted to evaluate the sensitivity and specificity of 
      microRNA-646 in diagnosing nasopharyngeal carcinoma. The overall survival of 
      patients with nasopharyngeal carcinoma was calculated based on their expression 
      levels of microRNA-646. The regulatory effects of microRNA-646 and mTOR on 
      proliferative potential and cell cycle progression were explored by cell counting 
      kit-8 (CCK-8) assay and flow cytometry, respectively. Dual-luciferase reporter 
      gene assay was conducted to verify the relationship between microRNA-646 and 
      mTOR, which was further confirmed by Pearson correlation analysis. Finally, 
      gain-of-function experiments were carried out to determine whether microRNA-646 
      could regulate the proliferative potential and cell cycle progression of 
      nasopharyngeal carcinoma cells by targeting mTOR. RESULTS: MicroRNA-646 was lowly 
      expressed in nasopharyngeal carcinoma tissues and cell lines. Survival analysis 
      confirmed the diagnostic value of microRNA-646 in nasopharyngeal carcinoma. 
      Besides, the nasopharyngeal carcinoma patients with high level of microRNA-646 
      were expected to have a longer 5-year survival time compared with those with low 
      level. Overexpression of microRNA-646 inhibited the proliferative potential and 
      cell cycle progression of HONE1 and SUNE1 nasopharyngeal carcinoma cells. 
      Dual-luciferase reporter gene assay detected the binding of microRNA-646 to mTOR. 
      Moreover, mTOR was highly expressed in nasopharyngeal carcinoma tissues and cell 
      lines. A negative correlation was found between microRNA-646 and mTOR. That is, 
      the overexpression of mTOR could reverse the inhibitory effects of microRNA-646 
      on the proliferative potential and cell cycle progression of HONE1 and SUNE1 
      cells. CONCLUSIONS: MicroRNA-646 remains a low level in nasopharyngeal carcinoma. 
      It inhibits the proliferative potential and cell cycle progression of 
      nasopharyngeal carcinoma cells by targeting mTOR. It can, therefore, inhibit the 
      development of nasopharyngeal carcinoma.
FAU - Song, Y-L
AU  - Song YL
AD  - Department of Otolaryngology, The Seventh People's Hospital of Jinan, Jinan, 
      China. 13953190521@163.com.
FAU - Pan, M-Z
AU  - Pan MZ
FAU - Wang, A-L
AU  - Wang AL
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (3' Untranslated Regions)
RN  - 0 (MIRN646 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  - 3' Untranslated Regions
MH  - Cell Cycle
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - MicroRNAs/*genetics
MH  - Nasopharyngeal Carcinoma/*genetics
MH  - Nasopharyngeal Neoplasms/*genetics
MH  - Survival Analysis
MH  - TOR Serine-Threonine Kinases/*genetics
EDAT- 2019/11/07 06:00
MHDA- 2020/10/21 06:00
CRDT- 2019/11/08 06:00
PHST- 2019/11/08 06:00 [entrez]
PHST- 2019/11/07 06:00 [pubmed]
PHST- 2020/10/21 06:00 [medline]
AID - 19286 [pii]
AID - 10.26355/eurrev_201910_19286 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Oct;23(20):8905-8912. doi: 
      10.26355/eurrev_201910_19286.