FAM64A是有丝分裂原生质转换的丝分裂诱导调节因子。在这里，我们发现FAM64A信使RNA（mRNA）和蛋白质表达水平在胃癌组织中高于正常粘膜（p <0.05）。FAM64A甲基化与FAM64A mRNA表达呈负相关（p <0.05）。FAM64A的差异表达基因主要涉及消化、钾转运或交换ATP酶、收缩纤维、内肽酶和胰排泄（p <0.05）。与FAM64A相关的基因主要分为泛素介导的蛋白质降解、细胞周期、染色体分离和有丝分裂、微管结合和组织、氨基酸代谢、细胞因子受体、脂滴、中枢神经系统和胶原三聚体（p < 0.05）。FAM64A蛋白在正常胃粘膜中的表达水平低于肠化生、腺瘤和原发性癌（p <0.05），与年龄、T期、淋巴和静脉侵袭、肿瘤、淋巴结、转移分期和分化呈负相关（p <0.05），并与胃癌患者有良好的总体生存相关。FAM64A的过表达通过EGFR/Akt/mTOR/NF-κB促进增殖、抗凋亡、迁移、侵袭和上皮间质转化，而FAM64A的敲除则产生相反效应。FAM64A还通过ING5通过直接或间接形成脂滴诱导化疗抵抗。这些结果表明，FAM64A表达升高可能导致侵袭性表型，从而引发胃癌发生和进展。因此，FAM64A可以被视为一种预后生物标志物和基因治疗靶点。© 2023 The Authors. 由Wiley Periodicals LLC发表的药物开发研究

FAM64A is a mitogen-induced regulator of the metaphase and anaphase transition. Here, we found that FAM64A messenger RNA (mRNA) and protein expression levels were higher in gastric cancer tissue than in normal mucosa (p < .05). FAM64A methylation was negatively correlated with FAM64A mRNA expression (p < .05). The differentially expressed genes of FAM64A were mainly involved in digestion, potassium transporting or exchanging ATPase, contractile fibers, endopeptidase, and pancreatic secretion (p < .05). The FAM64A-related genes were principally categorized into ubiquitin-mediated proteolysis, cell cycle, chromosome segregation and mitosis, microtubule binding and organization, metabolism of amino acids, cytokine receptors, lipid droplet, central nervous system, and collagen trimer (p < .05). FAM64A protein expression was lower in normal gastric mucosa than intestinal metaplasia, adenoma, and primary cancer (p < .05), negatively correlated with older age, T stage, lymphatic and venous invasion, tumor, node, metastasis stage, and dedifferentiation (p < .05), and associated with a favorable overall survival of gastric cancer patients. FAM64A overexpression promoted proliferation, antiapoptosis, migration, invasion, and epithelial-mesenchymal transition via the EGFR/Akt/mTOR/NF-κB, while the opposite effect was observed for FAM64A knockdown. FAM64A also induced chemoresistance directly or indirectly through lipid droplet formation via ING5. These results suggested that upregulation of FAM64A expression might induce aggressive phenotypes, leading to gastric carcinogenesis and its subsequent progression. Thus, FAM64A could be regarded as a prognosis biomarker and a target for gene therapy.© 2023 The Authors. Drug Development Research published by Wiley Periodicals LLC.