title: miR-205 promotes proliferation and invasion of laryngeal squamous cell carcinoma by suppressing CDK2AP1 expression.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Hematology, Wuhan Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan , China. ganyyjj33@163.com.
authors.forename: Gang
authors.initials: G
authors.lastname: Zhong
authors.affiliation: 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.
authors.forename: Xingao
authors.initials: X
authors.lastname: Xiong
mesh_terms: D014408:Biomarkers, Tumor; D015153:Blotting, Western; D002294:Carcinoma, Squamous Cell / Q000201:enzymology / Q000473:pathology*; D049109:Cell Proliferation / Q000235:genetics*; D019938:Cyclin D1 / Q000378:metabolism; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D016259:Genes, myc / Q000235:genetics; D056945:Hep G2 Cells; D006801:Humans; D007822:Laryngeal Neoplasms / Q000473:pathology*; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D009361:Neoplasm Invasiveness / Q000235:genetics; D061251:Primary Cell Culture; D060888:Real-Time Polymerase Chain Reaction; D013489:Suppression, Genetic / Q000235:genetics*; D025521:Tumor Suppressor Proteins / Q000235:genetics* / Q000378:metabolism
chemical_list: D014408:Biomarkers, Tumor; D019938:Cyclin D1; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9; D035683:MicroRNAs; D025521:Tumor Suppressor Proteins; C096151:CDK2AP1 protein, human; C534425:MIR205, human