Targeting YOD1 by RNA Interference Inhibits Proliferation and Migration of Human Oral Keratinocytes through Transforming Growth Factor-β3 Signaling Pathway
| Autor: | Gang Chen, Jia-Wei Hong, Zhen Ding, Heng-Xue Wang, Jun-Yu Shen, Qi Wang, Meng-Xue Li, Li-Chun Xu, Xing Ge, Xiao-Long Zhou |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Small interfering RNA Messenger RNA Gene knockdown General Immunology and Microbiology Cell growth Chemistry General Medicine Transfection General Biochemistry Genetics and Molecular Biology Cell biology 03 medical and health sciences 030104 developmental biology 0302 clinical medicine RNA interference 030220 oncology & carcinogenesis Signal transduction Transforming growth factor |
| Zdroj: | BioMed Research International. 2018:1-8 |
| ISSN: | 2314-6141 2314-6133 |
| DOI: | 10.1155/2018/6254308 |
| Popis: | Objective. We have identified a gene YOD1 encoding deubiquitinating enzyme (DUB) responsible for nonsyndromic cleft lip with or without cleft palate (NSCL/P). We aimed to determine the effects of YOD1 RNA interference (RNAi) on cell proliferation and migration, playing an important role in lip and palate formation, and to clarify whether the mechanisms involved TGF-β3 signaling associated with NSCL/P. Methods. RNAi was applied to construct vectors expressing YOD1 small interference RNAs (siRNAs). The vectors were transfected into the human oral keratinocytes (HOK) cells. The cell proliferation and migration were evaluated by the cell counting kit-8 (CCK-8) assay and wound healing assay, respectively. The mRNA levels were detected by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). The protein levels were investigated by western blotting. Results. The proliferation of YOD1 siRNA-transfected HOK cells was remarkably inhibited. The migration rate was significantly decreased in the YOD1 siRNA-transfected HOK cells. The TGF-β3 mRNA and protein levels were decreased significantly by siRNA-mediated knockdown of YOD1. YOD1 RNAi reduced the phosphor-Smad2/3 levels significantly. Conclusions. YOD1 RNAi may inhibit cell proliferation and migration associated with the pathogenesis of NSCL/P through TGF-β3 signaling. The study indicates a novel role of YOD1 in regulating TGF-β3 signaling to affect cell proliferation and migration resulting in NSCL/P. |
| Databáze: | OpenAIRE |
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