PMID- 29043013
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2045-3701 (Print)
IS  - 2045-3701 (Electronic)
IS  - 2045-3701 (Linking)
VI  - 7
DP  - 2017
TI  - miR-125a suppresses viability and glycolysis and induces apoptosis by targeting 
      Hexokinase 2 in laryngeal squamous cell carcinoma.
PG  - 51
LID - 10.1186/s13578-017-0178-y [doi]
LID - 51
AB  - BACKGROUND: miR-125a usually functions as a tumor suppressor in cancers. However, 
      the role of miR-125a in laryngeal squamous cell carcinoma (LSCC) has not been 
      determined. METHODS: qRT-PCR was applied to measure the expression of miR-125a 
      and HK2 mRNA in LSCC tissues and cells. CCK-8 kit and flow cytometry analysis 
      were performed to detect cell viability and apoptosis. Luciferase reporter assay 
      and RNA immunoprecipitation (RIP) were conducted to confirm the relationship 
      between miR-125a and HK2. Commercial test kits were used to determine the 
      concentrations of glucose and l-lactate. Xenograft in mice was constructed to 
      validate the function and mechanism of miR-125a in LSCC tumor growth. RESULTS: A 
      negative correlation was found between miR-125a expression and the level of 
      Hexokinase 2 (HK2) mRNA in LSCC tissues. Functional experiments found that 
      miR-125a inhibited viability and glycolysis and induced apoptosis in LSCC cells. 
      Similarly, HK2 downregulation led to viability and glycolysis inhibition and 
      induction of apoptosis in LSCC cells in vitro. Moreover, miR-125a overexpression 
      suppressed LSCC xenograft growth in vivo. Mechanically, HK2 was verified to be a 
      target of miR-125a by luciferase reporter assays and RNA immunoprecipitation 
      (RIP) assays. Furthermore, restored HK2 expression reversed miR-125a-mediated 
      proliferation and glycolysis inhibition and induction of apoptosis in LSCC cells. 
      CONCLUSIONS: miR-125a suppressed LSCC progression by targeting HK2 in vitro and 
      in vivo, suggesting that miR-125a may be a potential molecular target for LSCC 
      treatment.
FAU - Sun, Zhanwei
AU  - Sun Z
AD  - Department of Otolaryngology, Henan Provincial People's Hospital, People's 
      Hospital of Zhengzhou University, Zhengzhou, 450000 China. GRID: grid.414011.1
FAU - Zhang, Wenqi
AU  - Zhang W
AD  - Department of Otolaryngology, Henan Provincial People's Hospital, People's 
      Hospital of Zhengzhou University, Zhengzhou, 450000 China. GRID: grid.414011.1
AD  - Department of Otolaryngology, Henan Provincial People's Hospital, People's 
      Hospital of Zhengzhou University, No. 7 Weiwu Road, Zhengzhou, 450003 People's 
      Republic of China. GRID: grid.414011.1
FAU - Li, Qian
AU  - Li Q
AD  - Department of Otolaryngology, Henan Provincial People's Hospital, People's 
      Hospital of Zhengzhou University, Zhengzhou, 450000 China. GRID: grid.414011.1
LA  - eng
PT  - Journal Article
DEP - 20171005
PL  - England
TA  - Cell Biosci
JT  - Cell & bioscience
JID - 101561195
PMC - PMC5629811
OTO - NOTNLM
OT  - Apoptosis
OT  - Glycolysis
OT  - HK2
OT  - Proliferation
OT  - miR-125a
EDAT- 2017/10/19 06:00
MHDA- 2017/10/19 06:01
PMCR- 2017/10/05
CRDT- 2017/10/19 06:00
PHST- 2017/04/13 00:00 [received]
PHST- 2017/09/28 00:00 [accepted]
PHST- 2017/10/19 06:00 [entrez]
PHST- 2017/10/19 06:00 [pubmed]
PHST- 2017/10/19 06:01 [medline]
PHST- 2017/10/05 00:00 [pmc-release]
AID - 178 [pii]
AID - 10.1186/s13578-017-0178-y [doi]
PST - epublish
SO  - Cell Biosci. 2017 Oct 5;7:51. doi: 10.1186/s13578-017-0178-y. eCollection 2017.