PMID- 30664152
OWN - NLM
STAT- MEDLINE
DCOM- 20190520
LR  - 20211204
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 43
IP  - 3
DP  - 2019 Mar
TI  - miR‑122 and miR‑199 synergistically promote autophagy in oral lichen planus by 
      targeting the Akt/mTOR pathway.
PG  - 1373-1381
LID - 10.3892/ijmm.2019.4068 [doi]
AB  - The aim of the present study was to characterize the roles of two microRNAs 
      (miRNAs), miR‑122 and miR‑199, in oral lichen planus (OLP). miRNA microarray 
      analysis was performed to detect potential miRNAs involved in OLP, while 
      in‑silicon analysis, reverse transcription‑quantitative polymerase chain reaction 
      (RT‑qPCR), western blot and immunohistochemistry (IHC) analyses were utilized to 
      explore the molecular mechanisms underlying the roles of miR‑199 and miR‑122 in 
      OLP. The results from the microarray and RT‑qPCR analyses demonstrated that the 
      expression levels of miR‑122 and miR‑199 were significantly decreased in the 
      peripheral blood mononuclear cells (PBMCs) collected from the OLP group compared 
      with the control group. In addition, miR‑122 and miR‑199 directly targeted AKT 
      serine/threonine kinase 1 (AKT1) and mammalian target of rapamycin (mTOR), 
      respectively, by binding to their 3' UTRs. AKT1 and mTOR were highly expressed in 
      PBMCs derived from OLP patients. In fact, a negative regulatory relationship was 
      observed between miR‑122 and AKT1, and between miR‑199 and mTOR, with negative 
      correlation coefficients of ‑0.41 and ‑0.51, respectively. Furthermore, the 
      protein levels of AKT1, mTOR and microtubule associated protein 1 light chain 3beta 
      (LC3B) were upregulated in the OLP group compared with the control group. 
      Finally, overexpression of miR‑122 inhibited the expression of AKT1 and LC3B, 
      while overexpression of miR‑199 reduced the levels of mTOR and LC3B. In 
      conclusion, the present study demonstrated that miR‑199 and miR‑122 are 
      implicated in the pathogenesis of OLP by regulating the expression of mTOR and 
      AKT1.
FAU - Wang, Liang
AU  - Wang L
AD  - Department of Stomatology, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, P.R. 
      China.
FAU - Wu, Wei
AU  - Wu W
AD  - Department of Stomatology, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, P.R. 
      China.
FAU - Chen, Jijun
AU  - Chen J
AD  - Department of Stomatology, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, P.R. 
      China.
FAU - Li, Youhua
AU  - Li Y
AD  - Department of Stomatology, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, P.R. 
      China.
FAU - Xu, Ming
AU  - Xu M
AD  - Department of Stomatology, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, P.R. 
      China.
FAU - Cai, Yawei
AU  - Cai Y
AD  - Department of Geriatrics, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20190121
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (MIRN122 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (mirn199 microRNA, human)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Autophagy/*genetics
MH  - Cell Line
MH  - Female
MH  - Gene Expression Profiling
MH  - Gene Expression Regulation
MH  - Humans
MH  - Immunohistochemistry
MH  - Lichen Planus, Oral/*genetics/*metabolism/pathology
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Middle Aged
MH  - Proto-Oncogene Proteins c-akt/genetics/*metabolism
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/genetics/*metabolism
MH  - Young Adult
PMC - PMC6365087
EDAT- 2019/01/22 06:00
MHDA- 2019/05/21 06:00
PMCR- 2019/01/21
CRDT- 2019/01/22 06:00
PHST- 2018/03/31 00:00 [received]
PHST- 2018/12/31 00:00 [accepted]
PHST- 2019/01/22 06:00 [pubmed]
PHST- 2019/05/21 06:00 [medline]
PHST- 2019/01/22 06:00 [entrez]
PHST- 2019/01/21 00:00 [pmc-release]
AID - ijmm-43-03-1373 [pii]
AID - 10.3892/ijmm.2019.4068 [doi]
PST - ppublish
SO  - Int J Mol Med. 2019 Mar;43(3):1373-1381. doi: 10.3892/ijmm.2019.4068. Epub 2019 
      Jan 21.