PMID- 26515287
OWN - NLM
STAT- MEDLINE
DCOM- 20160519
LR  - 20181113
IS  - 0717-6287 (Electronic)
IS  - 0716-9760 (Print)
IS  - 0716-9760 (Linking)
VI  - 48
DP  - 2015 Oct 29
TI  - miR-205 promotes proliferation and invasion of laryngeal squamous cell carcinoma 
      by suppressing CDK2AP1 expression.
PG  - 60
LID - 10.1186/s40659-015-0052-5 [doi]
LID - 60
AB  - BACKGROUND: The aberrant expression of microRNAs (miRNAs) has been found in 
      various types of cancer. miR-205 was reported to be upregulated in laryngeal 
      squamous cell carcinoma (LSCC) tissues, however, the mechanisms by which miR-205 
      functions as a regulator of LSCC are largely unknown. RESULTS: In this study, 
      Real-time qPCR and Western blot assay showed that expression of miR-205 was 
      upregulated and expression of cyclin-dependent kinase 2-associated protein 1 
      (CDK2AP1) was downregulated in LSCC tissues. The expression levels of miR-205 
      were negatively related to those of CDK2AP1 in LSCC tissues and cell lines. 
      Moreover, we found that miR-205 was the upstream regulator of CDK2AP1 and could 
      suppress the CDK2AP1 expression in LSCC cells. 
      3-(4,5-dimethylthiazal-2-yl)-2,5-diphenyl-tetrazolium bromide assays and 
      transwell invasion assay were performed to test the proliferation and invasion of 
      LSCC cells. Gelatin zymography was used to detect the activity of MMP2 and MMP9. 
      CDK2AP1, c-Myc and CyclinD1 expression in cells was assessed with Western 
      blotting. We found that miR-205 was the upstream regulator of CDK2AP1 and could 
      suppress the expression of CDK2AP1 in LSCC cells. In addition, miR-205 
      significantly induced cell proliferation and invasion by suppressing CDK2AP1 
      expression. Consistent with miR-205 inhibitors, overexpressed CDK2AP1 suppressed 
      the activity of MMP2 and MMP9 and c-Myc and CyclinD1 expression in LSCC cells. 
      CONCLUSION: These findings help us to better elucidate the molecular mechanisms 
      of LSCC progression and provide a new theoretical basis to further investigate 
      miR-205 as a potential biomarker and a promising approach for LSCC treatment.
FAU - Zhong, Gang
AU  - Zhong G
AD  - Department of Hematology, Wuhan Union Hospital of Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan , China. ganyyjj33@163.com.
FAU - Xiong, Xingao
AU  - Xiong X
AD  - Department of Otolaryngology, Wuhan Union Hospital of Tongji Medical College, 
      Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, Hubei, 
      430022, China. xingaoxiong2133@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151029
PL  - England
TA  - Biol Res
JT  - Biological research
JID - 9308271
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (CDK2AP1 protein, human)
RN  - 0 (MIRN205 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 136601-57-5 (Cyclin D1)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Biomarkers, Tumor
MH  - Blotting, Western
MH  - Carcinoma, Squamous Cell/enzymology/*pathology
MH  - Cell Proliferation/*genetics
MH  - Cyclin D1/metabolism
MH  - Down-Regulation
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, myc/genetics
MH  - Hep G2 Cells
MH  - Humans
MH  - Laryngeal Neoplasms/*pathology
MH  - Matrix Metalloproteinase 2/metabolism
MH  - Matrix Metalloproteinase 9/metabolism
MH  - MicroRNAs/*genetics/metabolism
MH  - Neoplasm Invasiveness/genetics
MH  - Primary Cell Culture
MH  - Real-Time Polymerase Chain Reaction
MH  - Suppression, Genetic/*genetics
MH  - Tumor Suppressor Proteins/*genetics/metabolism
PMC - PMC4625464
EDAT- 2015/10/31 06:00
MHDA- 2016/05/20 06:00
PMCR- 2015/10/29
CRDT- 2015/10/31 06:00
PHST- 2015/07/02 00:00 [received]
PHST- 2015/10/20 00:00 [accepted]
PHST- 2015/10/31 06:00 [entrez]
PHST- 2015/10/31 06:00 [pubmed]
PHST- 2016/05/20 06:00 [medline]
PHST- 2015/10/29 00:00 [pmc-release]
AID - 10.1186/s40659-015-0052-5 [pii]
AID - 52 [pii]
AID - 10.1186/s40659-015-0052-5 [doi]
PST - epublish
SO  - Biol Res. 2015 Oct 29;48:60. doi: 10.1186/s40659-015-0052-5.