PMID- 25309979
OWN - NLM
STAT- MEDLINE
DCOM- 20150811
LR  - 20141114
IS  - 1791-2423 (Electronic)
IS  - 1019-6439 (Linking)
VI  - 46
IP  - 1
DP  - 2015 Jan
TI  - MicroRNA-93 regulates cyclin G2 expression and plays an oncogenic role in 
      laryngeal squamous cell carcinoma.
PG  - 161-74
LID - 10.3892/ijo.2014.2704 [doi]
AB  - microRNA93 (miR-93) is expressed in the miR‑106b-25 cluster, located in intron 13 
      of the MCM7 gene. Our previous study found that miR-93 was significantly 
      upregulated in laryngeal squamous cell carcinoma (LSCC), and cyclin G2 (CCNG2) 
      was a potential target of miR-93 in LSCC. However, the possible functions and 
      molecular mechanisms of miR-93 in LSCC remain unknown. In the present study, we 
      show that the level of CCNG2 protein expression was significantly lower in LSCC 
      cancer tissue than normal tissues. The level of CCNG2 was correlated with 
      clinical stages, lymph node metastasis and histological grade. We further show 
      that the expression level of miR-93 was inversely correlated with CCNG2 
      expression in clinical specimens. Furthermore, gain-of-function assays revealed 
      that miR-93 promoted cell proliferation, decreased apoptosis rates, induced cell 
      cycle arrest and promoted cell migration and invasion, whereas silencing of 
      miR-93 attenuated these carcinogenic processes. In addition, overexpression of 
      miR-93 in Hep-2 cells could reduce the mRNA and protein levels of CCNG2, whereas 
      silencing of miR-93 in Hep-2 cells significantly increased CCNG2 expression. A 
      luciferase assay verified that miR-93 could bind to the 3' untranslated region of 
      CCNG2. Importantly, ectopic expression of CCNG2 in miR-93 cells rescued the 
      effect of miR-93 on LSCC proliferation. Knockdown of CCNG2 promoted cell 
      proliferation resembling that of miR-93 overexpression. These findings 
      demonstrated that miR-93 promotes tumor growth by directly suppressing CCNG2. 
      Taken together, these results suggested that this newly identified miR-93-CCNG2 
      axis may be involved in LSCC proliferation and progression. Our findings provide 
      novel potential targets for LSCC therapy and prognosis.
FAU - Xiao, Xiyan
AU  - Xiao X
AD  - Department of Otolaryngology-Head and Neck Surgery, Fudan University Affiliated 
      Eye, Ear, Nose and Throat Hospital, Shanghai 200031, P.R. China.
FAU - Zhou, Liang
AU  - Zhou L
AD  - Department of Otolaryngology-Head and Neck Surgery, Fudan University Affiliated 
      Eye, Ear, Nose and Throat Hospital, Shanghai 200031, P.R. China.
FAU - Cao, Pengyu
AU  - Cao P
AD  - Department of Otolaryngology-Head and Neck Surgery, Fudan University Affiliated 
      Eye, Ear, Nose and Throat Hospital, Shanghai 200031, P.R. China.
FAU - Gong, Hongli
AU  - Gong H
AD  - Department of Otolaryngology-Head and Neck Surgery, Fudan University Affiliated 
      Eye, Ear, Nose and Throat Hospital, Shanghai 200031, P.R. China.
FAU - Zhang, Yanping
AU  - Zhang Y
AD  - Central Laboratory, Fudan University Affiliated Eye, Ear, Nose and Throat 
      Hospital, Shanghai 200031, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141010
PL  - Greece
TA  - Int J Oncol
JT  - International journal of oncology
JID - 9306042
RN  - 0 (CCNG2 protein, human)
RN  - 0 (Cyclin G2)
RN  - 0 (MIRN93 microRNA, human)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Animals
MH  - Carcinoma, Squamous Cell/*genetics/pathology
MH  - Cyclin G2/*genetics
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - HEK293 Cells
MH  - Humans
MH  - Laryngeal Neoplasms/*genetics/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - MicroRNAs/*physiology
MH  - Middle Aged
MH  - Oncogenes
MH  - Tumor Cells, Cultured
EDAT- 2014/10/14 06:00
MHDA- 2015/08/12 06:00
CRDT- 2014/10/14 06:00
PHST- 2014/08/13 00:00 [received]
PHST- 2014/09/22 00:00 [accepted]
PHST- 2014/10/14 06:00 [entrez]
PHST- 2014/10/14 06:00 [pubmed]
PHST- 2015/08/12 06:00 [medline]
AID - 10.3892/ijo.2014.2704 [doi]
PST - ppublish
SO  - Int J Oncol. 2015 Jan;46(1):161-74. doi: 10.3892/ijo.2014.2704. Epub 2014 Oct 10.