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

作者全名："Zhang, Duoli; Zou, Tao; Liu, Qingsong; Chen, Jie; Xiao, Mintao; Zheng, Anfu; Zhang, Zhuo; Du, Fukuan; Dai, Yalan; Xiang, Shixin; Wu, Xu; Li, Mingxing; Chen, Yu; Zhao, Yueshui; Shen, Jing; Chen, Guiquan; Xiao, Zhangang"

作者地址："[Zhang, Duoli; Zou, Tao; Chen, Jie; Xiao, Mintao; Zheng, Anfu; Zhang, Zhuo; Du, Fukuan; Wu, Xu; Li, Mingxing; Chen, Yu; Zhao, Yueshui; Shen, Jing; Xiao, Zhangang] Southwest Med Univ, Sch Pharm, Dept Pharmacol, Mol Pharmacol Lab, Luzhou, Peoples R China; [Liu, Qingsong] First Peoples Hosp Neijiang, Dept Pathol, Neijiang, Peoples R China; [Du, Fukuan; Li, Mingxing; Chen, Yu; Zhao, Yueshui; Shen, Jing; Xiao, Zhangang] Cell Therapy & Cell Drugs Luzhou Key Lab, Luzhou, Peoples R China; [Du, Fukuan; Li, Mingxing; Chen, Yu; Zhao, Yueshui; Shen, Jing; Xiao, Zhangang] South Sichuan Inst Translat Med, Luzhou, Sichuan, Peoples R China; [Dai, Yalan] Southwest Med Univ, Affiliated Hosp, Dept Oncol, Luzhou, Sichuan, Peoples R China; [Xiang, Shixin] Chongqing Med Univ, Univ Town Hosp, Dept Pharm, Chongqing, Peoples R China; [Chen, Guiquan] Southwest Med Univ, Chinese Med Hosp, Luzhou, Sichuan, Peoples R China"

通信作者："Xiao, ZG (通讯作者)，Southwest Med Univ, Sch Pharm, Dept Pharmacol, Mol Pharmacol Lab, Luzhou, Peoples R China.; Xiao, ZG (通讯作者)，Cell Therapy & Cell Drugs Luzhou Key Lab, Luzhou, Peoples R China.; Xiao, ZG (通讯作者)，South Sichuan Inst Translat Med, Luzhou, Sichuan, Peoples R China.; Chen, GQ (通讯作者)，Southwest Med Univ, Chinese Med Hosp, Luzhou, Sichuan, Peoples R China."

来源：PEERJ

ESI学科分类：Multidisciplinary

WOS号：WOS:001116947000003

JCR分区：Q2

影响因子：2.3

年份：2023

卷号：11

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：p53 signaling pathway; METTL7A; Melanoma; Immunomodulation

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."

基金机构："National Natural Science Foundation of China [81972643, 82172962]; Sichuan Science and Technology Project [2021YJ0201]; Luxian People's Government and Southwest Medical University Scientific and Technological Achievements Transfer and Transformation Strategic Cooperation Project [2019LXXNYKD-07]; Science and Technology Program of Luzhou, China [21CGZHPT0001]"

基金资助正文："This work was supported by the National Natural Science Foundation of China (No. 81972643, No. 82172962), the Sichuan Science and Technology Project (2021YJ0201), the Luxian People's Government and Southwest Medical University Scientific and Technological Achievements Transfer and Transformation Strategic Cooperation Project (2019LXXNYKD-07) and the Science and Technology Program of Luzhou, China (No. 21CGZHPT0001). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript."