PMID- 30868890
OWN - NLM
STAT- MEDLINE
DCOM- 20190912
LR  - 20190912
IS  - 0028-2685 (Print)
IS  - 0028-2685 (Linking)
VI  - 66
IP  - 4
DP  - 2019 Jul 23
TI  - MicroRNA-101 regulates autophagy, proliferation and apoptosis via targeting EZH2 
      in laryngeal squamous cell carcinoma.
PG  - 507-515
LID - 180811N611 [pii]
LID - 10.4149/neo_2018_180811N611 [doi]
AB  - Laryngeal carcinoma is the second commonest head and neck carcinoma globally. 
      MicroRNA-101 (miR-101) has been reported as a tumor suppressor in multiple 
      malignancies including laryngeal squamous cell carcinoma (LSCC). However, the 
      roles and molecular mechanisms of miR-101 in the development of LSCC have not 
      been fully elucidated. In present study, RT-qPCR assay was performed to detect 
      the expression of miR-101 and enhancer of zeste homolog 2 (EZH2) mRNA. Western 
      blot assay was conducted to determine protein expression of LC3-Ⅰ, LC3-Ⅱ, p62 and 
      EZH2. Cell proliferative capacity was evaluated by MTS assay. The effect of 
      miR-101 alone or along with EZH2 on cell apoptosis was assessed by apoptotic 
      index and caspase-3 activity. Bioinformatic analysis, luciferase assay and RNA 
      immunoprecipitation (RIP) assay were carried out to investigate the interaction 
      between miR-101 and EZH2. Results revealed that miR-101 expression was strikingly 
      down-regulated in LSCC cell lines. Functional analyses showed that ectopic 
      expression of miR-101 suppressed cell autophagy and proliferation and facilitated 
      cell apoptosis in LSCC. Further investigations revealed that miR-101 inhibited 
      EZH2 expression by direct interaction and EZH2 was highly expressed in LSCC 
      cells. Also, EZH2 knockdown reduced the autophagic activity of LSCC cells. 
      Moreover, restoration experiments showed that EZH2 up-regulation weakened 
      miR-101-mediated anti-autophagy, anti-proliferation and pro-apoptosis effects in 
      LSCC cells. In conclusion, our findings suggested that miR-101 inhibited 
      autophagy and proliferation and promoted apoptosis via targeting EZH2 in LSCC, 
      providing a deep insight into the pathogenesis of LSCC and hinting the pivotal 
      roles of epigenetic modifications especially histone methylation in the 
      development of LSCC.
FAU - Chen, L
AU  - Chen L
AD  - Department of Otolaryngology, Henan Provincial People's Hospital, People's 
      Hospital of Zhengzhou University, Zhengzhou, China.
FAU - Jia, J
AU  - Jia J
AD  - Department of Otolaryngology, People's Hospital of Xixian, People's Hospital of 
      Zhengzhou University, Xinyang, China.
FAU - Zang, Y
AU  - Zang Y
AD  - Department of Otolaryngology, Henan Provincial People's Hospital, People's 
      Hospital of Zhengzhou University, Zhengzhou, China.
FAU - Li, J
AU  - Li J
AD  - Department of Otolaryngology, Henan Provincial People's Hospital, People's 
      Hospital of Zhengzhou University, Zhengzhou, China.
FAU - Wan, B
AU  - Wan B
AD  - Department of Otolaryngology, Henan Provincial People's Hospital, People's 
      Hospital of Zhengzhou University, Zhengzhou, China.
LA  - eng
PT  - Journal Article
DEP - 20190307
PL  - Slovakia
TA  - Neoplasma
JT  - Neoplasma
JID - 0377266
RN  - 0 (MIRN101 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - EC 2.1.1.43 (EZH2 protein, human)
RN  - EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein)
SB  - IM
MH  - *Apoptosis
MH  - *Autophagy
MH  - Carcinoma, Squamous Cell/*genetics/pathology
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Enhancer of Zeste Homolog 2 Protein/*genetics
MH  - Epigenesis, Genetic
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Laryngeal Neoplasms/*genetics/pathology
MH  - MicroRNAs/*genetics
EDAT- 2019/03/15 06:00
MHDA- 2019/09/13 06:00
CRDT- 2019/03/15 06:00
PHST- 2018/08/11 00:00 [received]
PHST- 2018/12/19 00:00 [accepted]
PHST- 2019/03/15 06:00 [pubmed]
PHST- 2019/09/13 06:00 [medline]
PHST- 2019/03/15 06:00 [entrez]
AID - 180811N611 [pii]
AID - 10.4149/neo_2018_180811N611 [doi]
PST - ppublish
SO  - Neoplasma. 2019 Jul 23;66(4):507-515. doi: 10.4149/neo_2018_180811N611. Epub 2019 
      Mar 7.