机构：[1]Department of Endodontics, Hebei Key Laboratory of Stomatology, Hebei Clinical Research Center for Oral Diseases, School and Hospital of Stomatology, Hebei Medical University, 383# Zhong Shan East Road, Shijiazhuang, Hebei 50017, China.[2]Department of Oral and Maxillofacial, The Fourth Hospital of Hebei Medical University and Hebei Tumor Hospital, Hebei Medical University, 12#, JianKang Road, Shijiazhuang, Hebei 50017, China.河北医科大学第四医院[3]Department of Pathology, Hebei Key Laboratory of Stomatology, Hebei Clinical Research Center for Oral Diseases, School and Hospital of Stomatology, Hebei Medical University, 383# Zhong Shan East Road, Shijiazhuang, Hebei 50017, China.[4]Department of Oral and Maxillofacial, Hebei Key Laboratory of Stomatology, Hebei Clinical Research Center for Oral Diseases, School and Hospital of Stomatology, Hebei Medical University, 383# Zhong Shan East Road, Shijiazhuang, Hebei 50017, China.
Oral squamous cell carcinoma (OSCC) still threatens people's daily life. METTL14 is a newly discovered methyltransferase that catalyzes m6A methylation. Hence, this research was carried out to investigate the action mechanism of METTL14 in OSCC. The SCC-4 and UM2 cells, and tumorigenicity assay were utilized to investigate METTL14 roles in vitro and in vivo. Bioinformatic analysis was carried out with the UCSC, TCGA database and The Human Protein Atlas. The gene expression at mRNA and protein levels were measured by qRT-PCR and Western blot. In addition, cell growth and metastasis was analyzed by colony formation and transwell assays. MeRIP assay was performed to test the m6A levels of CALD1. The METTL14 and CALD1 levels were prominently expressed in OSCC cells. METTL14 silencing depleted the cell growth and metastasis. Furthermore, METTL14 silencing depleted the tumor growth in vivo. Additionally, the mRNA and m6A levels of CALD1 were depleted after METTL14 silencing. Overexpressed CALD1 neutralized the si-METTL14 effects in OSCC cells. In conclusion, METTL14 participated in the OSCC progression through modulating the mRNA and m6A levels of CALD1.
第一作者机构：[1]Department of Endodontics, Hebei Key Laboratory of Stomatology, Hebei Clinical Research Center for Oral Diseases, School and Hospital of Stomatology, Hebei Medical University, 383# Zhong Shan East Road, Shijiazhuang, Hebei 50017, China.
推荐引用方式(GB/T 7714)：
Chen Ruixue,Zhang Suxin,Li Hexiang,et al.METTL14 Promotes Oral Squamous Cell Carcinoma Progression by Regulating the mRNA and m6A Levels of CALD1[J].JOURNAL OF ENVIRONMENTAL PATHOLOGY TOXICOLOGY AND ONCOLOGY.2023,42(3):71-81.doi:10.1615/JEnvironPatholToxicolOncol.2022045134.
APA：
Chen Ruixue,Zhang Suxin,Li Hexiang,Yang Mengyuan,Lu Yiwen&Zhang Xudong.(2023).METTL14 Promotes Oral Squamous Cell Carcinoma Progression by Regulating the mRNA and m6A Levels of CALD1.JOURNAL OF ENVIRONMENTAL PATHOLOGY TOXICOLOGY AND ONCOLOGY,42,(3)
MLA：
Chen Ruixue,et al."METTL14 Promotes Oral Squamous Cell Carcinoma Progression by Regulating the mRNA and m6A Levels of CALD1".JOURNAL OF ENVIRONMENTAL PATHOLOGY TOXICOLOGY AND ONCOLOGY 42..3(2023):71-81
