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자료유형
학술저널
저자정보
Geng Ya-Wei (The Second Affiliated Hospital of Harbin Medical University China) Zhang Zhen (The Second Affiliated Hospital of Harbin Medical University China) Jin Han (The Second Affiliated Hospital of Harbin Medical University China) Da Jun-Long (The Second Affiliated Hospital of Harbin Medical University China) Zhang Kai (The Second Affiliated Hospital of Harbin Medical University China) Wang Jian-Qun (The Second Affiliated Hospital of Harbin Medical University China) Guo Yu-Yao (The Second Affiliated Hospital of Harbin Medical University China) Zhang Bin (The Second Affiliated Hospital of Harbin Medical University China) Li Ying (The Second Affiliated Hospital of Harbin Medical University China)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.44 No.2
발행연도
2022.2
수록면
155 - 164 (10page)
DOI
10.1007/s13258-021-01170-4

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Background Fam20c is intimately related to tissue development and diseases. At present, it has been reported that Fam20c regulates the mineralization of osteoblasts, but there are few reports on other effects. Objective To study the effect of Fam20c on osteoblasts by knocking out the Fam20c gene. Methods Fam20c knockout osteoblasts were constructed by transfecting mouse osteoblasts with lentivirus. The proliferation, migration and mineralization of Fam20c knockout cells were detected by CCK-8, scratch test and alizarin red staining assays. The subcellular structure was observed by transmission electron microscopy. RT?PCR was used to detect the differential expression of mesenchymal-to-epithelial transition (MET)-related marker genes and core transcription factors. The differential expression of MET-related proteins was detected by immunofluorescence or Western blot. Transcriptome analysis of Fam20c knockout osteoblasts was performed, and real-time PCR was used to verify transcriptome analysis related to MET. Results The proliferation ability of osteoblasts was not significantly changed after Fam20c deletion, but the migration ability and mineralization ability were significantly weakened. There were tight junctions between Fam20c knockout cells. The expression of mesenchymal cell marker genes and core transcription factors was significantly decreased, and the expression of epithelial cell marker genes was significantly increased. The expression of mesenchymal cell marker proteins was significantly decreased, and the expression of epithelial cell marker proteins was significantly increased. Multiple signalling molecules and pathways involved in MET have changed. Conclusions Knockdown of Fam20c resulted in MET. Fam20c affects the transcription of key factors in osteoblast MET.

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