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Transcriptomic characterization revealed that METTL7A inhibits melanoma progression via the p53 signaling pathway and immunomodulatory pathway

基因敲除 癌症研究 黑色素瘤 生物 信号转导 生物信息学 下调和上调 转录组 免疫疗法 表型 癌细胞 免疫系统 癌症 基因 基因表达 免疫学 细胞生物学 遗传学
作者
Duoli Zhang,Tao Zou,Qingsong Liu,Jie Chen,Mintao Xiao,Anfu Zheng,Zhuo Zhang,Fukuan Du,Yalan Dai,Shixin Xiang,Xu Wu,Mingxing Li,Yu Chen,Yueshui Zhao,Jing Shen,Guiquan Chen,Zhangang Xiao
出处
期刊:PeerJ [PeerJ, Inc.]
卷期号:11: e15799-e15799 被引量:3
标识
DOI:10.7717/peerj.15799
摘要

METTL7A is a protein-coding gene expected to be associated with methylation, and its expression disorder is associated with a range of diseases. However, few research have been carried out to explore the relationship between METTL7A and tumor malignant phenotype as well as the involvement potential mechanism. We conducted our research via a combination of silico analysis and molecular biology techniques to investigate the biological function of METTL7A in the progression of cancer. Gene expression and clinical information were extracted from the TCGA database to explore expression variation and prognostic value of METTL7A. In vitro , CCK8, transwell, wound healing and colony formation assays were conducted to explore the biological functions of METT7A in cancer cell. GSEA was performed to explore the signaling pathway involved in METTL7A and validated via western blotting. In conclusion, METTL7A was downregulated in most cancer tissues and its low expression was associated with shorter overall survival. In melanoma, METTL7A downregulation was associated with poorer clinical staging, lower levels of TIL infiltration, higher IC50 levels of chemotherapeutic agents, and poorer immunotherapy outcomes. QPCR results confirm that METTL7A is down-regulated in melanoma cells. Cell function assays showed that METTL7A knockdown promoted proliferation, invasion, migration and clone formation of melanoma cells. Mechanistic studies showed that METTL7A inhibits tumorigenicity through the p53 signaling pathway. Meanwhile, METTL7A is also a potential immune regulatory factor.
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