目的 观察低氧对p53RFP基因表达及启动子活性的影响,探索低氧反应元件(HRE)是否参与了低氧对p53RFP基因启动子活性的调控。方法 将HEK293细胞置于低氧条件下培养,实时定量PCR及Western blot 检测p53RFP mRNA及蛋白表达水平;通过定点突变技术构建HRE突变型p53RFP启动子双荧光素酶报告基因载体并转染HEK293细胞,分别置于常氧和低氧条件下培养,双荧光素酶报告基因检测系统检测启动子活性。结果 低氧处理不同时间点p53RFP mRNA 表达水平均显著增加,差异有统计学意义(F=96.493,P<0.001);低氧组p53RFP 及HIF-1α蛋白表达量均呈时间依赖性递增。成功构建了HRE 突变型p53RFP 启动子双荧光素酶报告基因载体,双荧光素酶报告基因检测显示,与常氧组相比,低氧条件下野生型p53RFP基因启动子活性增加(t=-19.504,P<0.001),HRE单突变或双突变后启动子活性均较野生型降低(F=160.891,P<0.001)。结论 低氧可诱导p53RFP基因表达上调;成功构建了HRE 突变型p53RFP 双荧光素酶报告基因载体,HRE 位点可能在低氧调控p53RFP基因启动子活性中发挥关键作用。

Objective To investigate the effect of hypoxia on p53RFP gene expression and p53RFP promoter activity, and explore whether hypoxia responsive element (HRE) is involved in the regulation of p53RFP gene promoter activity by hypoxia. Methods HEK293 cells were cultured under normoxia and hypoxia conditions, p53RFP expressions at mRNA and protein levels were detected by real-time PCR and Western blot respectively. The HRE mutant p53RFP promoter dual luciferase reporter gene vector was constructed by site-directed mutagenesis technology and transfected into HEK293 cells under normoxia and hypoxia conditions. The promoter activities were detected by dual luciferase reporter system. Results Compared with the normoxia group, the expression of p53RFP mRNA in the hypoxia group increased significantly at different time points, and the difference was statistically significant(F=96.493,P<0.001); the expression of p53RFP and HIF-1α protein in the hypoxia group increased in a time-dependent manner. The luciferase reporter vectors containing p53RFP with mutant HRE were successfully constructed. The dual luciferase reporter gene assay showed that the activity of the wild-type p53RFP gene promoter was significantly increased under hypoxic conditions compared to normoxic condition(t=-19.504,P<0.001),and the promoter activity of p53RFP with HRE single mutation or double mutation were both significantly lower than that of wild type under hypoxic condition (F=160.891,P<0.001). Conclusions p53RFP gene expression was induced by hypoxia; the p53RFP promoter with mutant HRE dual luciferase reporter gene vectors were successfully constructed, and the HRE locus may play a key role in the hypoxia regulation of p53RFP gene promoter activity.

非酒精性脂肪性肝病(NAFLD)是世界范围内慢性肝病的一个主要原因,约15%的NAFLD患者会发展为非酒精性脂肪性肝炎、肝纤维化、肝硬化甚至肝癌。目前其发病及进展机制尚未明确,也无有效治疗手段。因此,构建临床前NAFLD动物模型至关重要,有助于为NAFLD提供临床治疗的新方案。本文将系统分析目前已构建的NAFLD动物模型在临床前研究中的局限性,并重点总结和综述基于基因编辑在NAFLD动物模型构建中的应用及研究进展,这对于探讨NAFLD发病机制及新药研发具有重要的临床意义。

Nonalcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease worldwide, and about 15% of NAFLD patients will develop into nonalcoholic steatohepatitis, hepatic fibrosis, cirrhosis, and ultimately hepatocellular carcinoma. However, the biological mechanism of the pathogenesis and progression of NAFLD is not fully understood, and there are still no effective or targeted therapies for NAFLD. Therefore, it is an urgent need to construct pre-clinical animal models of NAFLD, which will help to better understand and explore the potential therapeutic strategy in the treatment of NAFLD. Here, we summarize the recent advances and limitations of the established animal models of NAFLD and focus on the potential application and research progress of genome editing for constructing the animal models of NAFLD. There animal models will be very useful to reveal the pathologic mechanism of human NAFLD, and to screen new therapeutic drugs.

融合基因是指两个独立基因的编码区首尾相连所形成的且置于同一套调控序列控制的产物,研究表明许多癌症的发生与融合基因存在密切的联系。融合基因可作为癌症治疗的靶点,在癌症诊断及治疗领域中融合基因的研究具有重要意义。部分融合基因驱动癌症的机制已被初步揭示,但是有些真实存在的在肿瘤发生发展过程中有重要意义的融合基因由于工具和实验技术限制还未被发现。因此,对融合基因的分析预测研究方法逐渐成为关注的热点之一。本文探讨了目前常用的关于融合基因的分析工具及方法,为融合基因在癌症中的研究提供思路。

Fusion genes are the products of two independent genes whose coding regions are linked and controlled by the same set of regulatory sequences．Studies have shown that many cancers are closely linked to gene fusions．Fusion genes can be used as targets for cancer therapy,and the study of fusion genes is of great importance in cancer diagnosis and treatment．Some of the mechanisms of fusion genes driving cancer have been initially revealed,but there are more fusion genes which are important in the process of tumor development have not been discovered due to the limitation of tools and experimental techniques．Therefore,the analysis and prediction methods of fusion genes are becoming a hot topic of interest．In this paper,we discuss the commonly used analytical tools and methods on fusion genes to provide ideas for the study of fusion genes in cancer．

嵌合基因是指由两个或多个原本不连续的基因片段重组而成的新基因,它们可以通过基因组重排、转录诱导等机制产生。嵌合基因在正常生理和发育过程中具有重要的功能和调控作用。嵌合基因可以改变原有基因的表达水平、编码蛋白质的结构和功能、信号通路的激活和抑制等,从而促进肿瘤细胞的增殖、侵袭、转移和耐药性。近年来,随着高通量测序技术的发展和应用,越来越多的嵌合基因被发现和鉴定,它们在不同类型的肿瘤中具有不同的表达模式和功能作用,为肿瘤的分子诊断、预后评估和靶向治疗提供了新的机会和挑战。本文旨在对嵌合基因产生的机制、检测方法和在肿瘤中的功能和应用等方面进行综述,为进一步认识嵌合基因在肿瘤进展中的功能机制及其精准化治疗提供参考。

Chimeric genes refer to novel genes formed by the recombination of two or more originally non-contiguous gene fragments through mechanisms like genomic rearrangement and transcriptional induction．They play important roles in physiological and developmental regulation．Chimeric genes can alter the expression,structure and function of original genes,modulate signaling pathway activation and inhibition,and thereby promote tumor cell proliferation,invasion,metastasis and drug resistance．In recent years,with the development and application of high-throughput sequencing technologies,increasing numbers of chimeric genes have been discovered and identified．They demonstrate different expression patterns and functional roles in various tumor types,providing new opportunities and challenges for molecular diagnosis,prognostic assessment and targeted therapy of cancers．This review summarizes the mechanisms of chimeric gene formation,detection methods and their functions and applications in tumors,to provide insights into the functional mechanisms of chimeric genes in tumor progression and their implications for precision treatment．

目的 探讨急性心肌梗死患者细胞色素P450酶基因(cytochrome P450,family 2,subfamily C,polypeptide 19,CYP2C19)多态性与高敏C-反应蛋白(hypersensitive C-reactive protein,hs-CRP)、白细胞介素-6(interleukin- 6,IL-6)及临床预后的相关性。方法 选取2019年5月—2020年5月入住我院心血管内科的急性心肌梗死患者182例作为研究对象,研究对象均接受经皮冠脉介入术,采取RT-PCR方法进行外周全血CYP2C19基因多态性的检测,并进行分组。口服阿司匹林300 mg和氯吡格雷300 mg后次日,测定血中hs-CRP和IL-6含量,治疗后12个月内,随访主要心血管不良事件。结果 182例急性心肌梗死患者中,快代谢组(CYP2C19*1/*1)患者最多,为78例(42.8%);中等代谢组(CYP2C19*1/*2、CYP2C19*1/*3),为65例(35.7%);慢代谢型组(CYP2C19*2/*2、CYP2C19*2/*3、CYP2C19*3/*3)最少,为39例(21.5%)。与快代谢组比较,中代谢组及慢代谢组hs-CRP、IL-6水平均升高,差异有统计学意义(P<0.05);与中代谢组比较,慢代谢组患者hs-CRP、IL-6水平均升高,差异有统计学意义(P<0.05)。CYP2C19基因型与hs-CRP及IL-6呈正相关(r=0.163、0.175,P<0.05)。中代谢组、慢代谢组患者1年内主要心血管不良事件发生率高于快代谢组患者(P<0.05)。结论 CYP2C19基因型与hs-CRP及IL-6具有相关性,CYP2C19基因型为中代谢型和慢代谢型能够激活机体炎症反应,影响急性心肌梗死患者的临床预后。

Objective To explore the correlation of cytochrome P450 gene (CYP2C19) polymorphism with hypersensitive C-reaction protein (hs-CRP), interleukin-6 (IL-6) and prognosis in patients with acute myocardial infarction (AMI). Methods A total of 182 patients with AMI admitted to cardiology department from May 2019 to May 2020 were selected as the research objects, all subjects underwent percutaneous coronary intervention (PCI), and CYP2C19 gene polymorphism in peripheral blood was detected by RT-PCR, which was grouping basis. One day after taking aspirin 300 mg and clopidogrel 300 mg orally, the levels of hs-CRP and IL-6 in patients' plasma were measured. The major adverse cardiovascular events (MACE) were followed up for 12 months after treatment. Results Among 182 patients with AMI, 78 patients (42.8%) were in the fast metabolism group (CYP2C19*1/*1), 65 patients (35.7%) in medium metabolism group (CYP2C19*1/*2, CYP2C19*1/*3), 39 patients (21.5%) in the slow metabolism group (CYP2C19*2/*2, CYP2C19*2/*3, CYP2C19*3/*3).Compared with the fast metabolism group, hs-CRP and IL-6 levels in the medium and slow metabolism group were significantly higher (P<0.05); compared with the medium metabolism group, hs-CRP and IL-6 levels in the slow metabolism group were significantly increased (P<0.05). CYP2C19 genotype was positively correlated with hs-CRP and IL-6 levels (r=0.163, 0.175,P<0.05). The incidences of MACE in the medium and slow metabolism groups were higher than that in the fast metabolism group (P<0.05). Conclusion CYP2C19 genotypes were associated with hs-CRP and IL-6 levels. Medium and slow metabolism types of CYP2C19 gene can activate the inflammatory response and affect the clinical prognosis of patients with AMI.

目的 探讨核结合蛋白2(NUCB2)介导的下游信号分子和通路,为阐明NUCB2在乳腺癌中的功能提供依据。方法 构建NUCB2-RNAi慢病毒载体,感染MDA-MB-231细胞株。然后将MDA-MB-231分为阴性对照病毒感染细胞组(NC组)、感染NUCB2基因shRNA病毒细胞组(KD组),用Affymetrix基因表达谱芯片对NUCB2下游基因进行筛选,并对所有数据进行独创性通路分析(IPA)分析。用qPCR测定mRNA水平。统计采用SPSS 20.0软件。结果 Path-Array研究筛选了KD组与NC组的差异基因,其中上调基因186个,下调基因356个,部分差异表达基因的检测表明,这些基因的mRNA水平与Path-Array筛选结果一致。IPA分析显示,经典途径中差异表达基因的显著富集表明胆固醇生物合成的超途径被显著抑制。上游调节因子分析显示了所有不同表达基因的上游调节因子,包括转录因子、细胞因子、小RNA、受体、激酶、化学分子和药物。疾病和功能差异表达基因的显著丰富表明,与NUCB2相关的差异表达基因与41种疾病和功能显著相关,更多与癌症、组织损伤和异常相关。结论 NUCB2的功能涉及多种基因和多种信号通路。

Objective In order to further explore the downstream signal molecules and pathways mediated by nucleobindin-2 (NUCB2), to provide a basis for elucidating the significance of NUCB2 in breast cancer. Method NUCB2-RNAi lentivirus vector was constructed and infecting MDA-MB-231 cell line.Then MDA-MB-231 cells were divived into two group, cells with negative control virus infection (NC group) and cells infected with NUCB2 gene shRNA virus (KD group). NUCB2 downstream gene screening was conducted by Affymetrix gene expression profiling Path-Array chip and all data were analyzed by ingenuity pathway analysis (IPA). The mRNA level was detected by qPCR. SPSS 20.0 software was used for statistics. Results Path-Array study screened out differential genes between KD and NC group which the number of up-regulated genes was 186, the number of down-regulated genes was 356.Detection of some differentially expressed genes showed that the mRNA levels of these genes were consistent with the results of Path-Array screening.IPA analysis revealed that significant enrichment of differentially expressed genes in the classical pathway showed superpathway of cholesterol biosynthesis was significantly inhibited.The upstream regulatory factor analysis showed the upstream regulatory factors of all the differentially expressed genes, including transcription factors, cytokine, small RNA, receptors, kinases, chemical molecules and drugs.The significant enrichment of differentially expressed genes in disease and function showed that NUCB2 associated differentially expressed genes were significantly related with 41 diseases and functions, which were more related with cancer, organismal injury and abnormities. Conclusion The function of NUCB2 involved multiple genes and multiple signaling pathways.

目的 分析ABCC2基因表达水平与肺腺癌预后之间的关联性,并对其影响机制进行初步探索。 方法 采用TCGA数据库和HPA数据库对肺腺癌病人癌组织和癌旁组织基因表达数据进行差异性分析,单因素及多因素COX回归评估ABCC2与肺腺癌预后之间的关联性,GSEA用于探讨与ABCC2显著关联的信号通路。 结果 ABCC2在肺腺癌肿瘤组织中存在过表达现象,Kaplan-Meier生存分析曲线结果显示ABCC2基因过表达使肺腺癌病人的死亡风险显著升高(HR=1.46,95%CI=1.09~1.95; P=0.010)。单因素及多因素COX回归结果显示ABCC2基因过表达是肺腺癌病人不良预后的独立危险因素。GSEA结果显示ABCC2可能通过调节药物代谢从而对肺腺癌的发展进行调控。 结论 ABCC2基因过表达使肺腺癌病人的死亡风险显著升高,ABCC2可能是肺腺癌不良预后的潜在分子生物标志物。

Objective To estimate the association between ABCC2 mRNA expression and the prognosis of lung adenocarcinoma and explore the potential influencing mechanism.Methods Difference analysis was used to evaluate the gene expression in tumor tissues and adjacent normal tissues based on The Cancer Genome Atlas database and Human Protein Atlas database.Multivariate COX regression and Kaplan-Meier analysis were performed to evaluate the association between ABCC2 gene expression and the prognosis of lung adenocarcinoma.Gene-set enrichment analysis (GSEA) was performed to screen differentially enriched pathways associated with the ABCC2 high expression phenotype.Results ABCC2 was overexpressed in lung adenocarcinoma tumor tissues compared with adjacent normal tissues.Kaplan-Meier survival analysis showed a significant relationship between ABCC2 mRNA expression and lung adenocarcinoma prognosis (HR=1.16,95% CI=1.09-1.95; P=0.010).Univariate and multivariate Cox regression analysis showed that ABCC2 mRNA expression was an independent risk factor affecting the survival of patients with lung adenocarcinoma.The results of GSEA suggested that ABCC2 may influence the development of lung adenocarcinoma by regulating the metabolism of targeted drug the treatment.Conclusions ABCC2 overexpression can significantly increase the risk of death in patients with lung adenocarcinoma,ABCC2 may be a potential molecular marker for poor prognosis in lung adenocarcinoma.

目的 乳腺癌是世界范围内最常见的恶性肿瘤之一。目前,人们对乳腺癌的发病机制进行了大量的研究,但对其分子机制的认识尚不清楚。本研究采用生物信息学技术,筛选乳腺癌潜在的关键基因,最终为乳腺癌的诊断、治疗及预后判断提供潜在的生物标记物。方法 从基因表达综合数据库(GEO)下载基因芯片GSE36295、GSE71053和GSE86374,通过GEO2R鉴定差异表达基因(DEGs),并进行功能富集分析。利用STRING构建了蛋白质-蛋白质相互作用网络(PPI),并采用Cytoscape进行了模块分析。结果 共鉴定出95个DEGs,包括62个上调基因和33个下调基因。共鉴定出10个Hub基因:CENPF、KIF2C、TOP2A、NUSAP1、HMMR、MELK、KIF4A、ASPM、CEP55、CCNB1。结论 本研究发现的Hub基因可能对乳腺癌的发展和预后存在一定影响,为乳腺癌的诊断和治疗提供候选靶点。

Objective Breast cancer is one of the most common cancers worldwide. At present, a lot of researches have been carried out on the pathogenesis of breast cancer, but the molecular mechanisms of breast cancer are still not well understood. In this study, bioinformatics technology was used to screen the potential key genes of breast cancer, and ultimately to provide potential biomarkers for the diagnosis, treatment and prognosis of breast cancer. Methods The microarray datasets GSE36295、GSE71053和GSE86374 were downloaded from Gene Expression Omnibus (GEO), and the differentially expressed genes (DEGs) were identified by GEO2R, and the enriched functions and pathways of the DEGs were analyzed. Protein-protein interaction network (PPI) was constructed by using String, and the module analysis was performed using Cytoscape. Results A total of 95 DEGs were identified, consisting of 62 upregulated genes and 33 downregulated genes.Ten hub genes were identified: CENPF,KIF2C,TOP2A,NUSAP1,HMMR,MELK,KIF4A,ASPM,CEP55,CCNB1. Conclusion The hub gene was found in this study may be involved in the development and prognosis of breast cancer. It may provide candidate targets for diagnosis and treatment of breast cancer.

目的 观察新疆石河子地区绝经后女性2型糖尿病(T2DM)患者糖、脂、骨代谢特征及骨密度(BMD)情况,探讨该人群中低密度脂蛋白受体相关蛋白5(LRP5)基因rs3736228、rs3781586位点的基因多态性及突变与糖、脂、骨代谢指标的关系。方法 将新疆石河子地区2016年10月—2017年10月社区、医院门诊及住院绝经后女性按照纳入标准和排除标准选取136例为研究对象,根据患者病史、糖耐量实验及骨密度仪测定骨密度分4组,糖耐量正常与骨量正常组(A组),糖耐量正常与骨量异常组(B组),T2DM与骨量正常组(C组),T2DM与骨量异常组(D组)。测定并记录患者年龄、绝经年限等基线资料,计算体质指数(BMI)等,并检测糖代谢指标(空腹血糖等)、骨代谢指标(血Ca等)、脂代谢指标(甘油三酯等)。采用MALDI-TOF-MS法测定LRP5基因该两个位点基因多态性并进行统计分析。结果 ①糖代谢指标:与A组比较,C组、D组FPG、HbA1c均高于A组(P<0.01)。脂代谢指标:与A组比较,B组、D组TG低于A组(P<0.05)。骨代谢指标:与A组比较,B组、D组BMD(L1-4)、BMD(股骨颈)低于A组(P<0.01)。②LRP5基因该两个位点SNP基因分型分布符合Hardy-Weinberg遗传平衡定律(P>0.05);同时,该两个位点不同基因型的分布频率和等位基因频率在组间的比较经Pearson Chi-Square检验后发现暂无显著差异(P>0.05)。③LRP5基因rs3736228位点:A组,与CC型(野生型)相比,CT/TT型(突变型)甘油三酯(TG)降低(P<0.05),BMD(L1-4)降低(P<0.05);C组,与CC型(野生型)相比,CT/TT型(突变型)高密度脂蛋白(HDL-C)升高(P<0.01),磷(P)升高(P<0.05);LRP5基因rs3781586位点:B组,与GG型(野生型)相比,GT/TT(突变型)高密度脂蛋白(HDL-C)升高(P<0.05)。结论 在新疆石河子地区绝经后女性2型糖尿病人群中,LRP5基因rs3736228、rs3781586位点的基因多态性可能与糖代谢无关,但LRP5基因rs3736228位点的突变可能与脂代谢(TG、HDL-C)、骨代谢(P、BMD)有关,rs3781586位点的突变可能与脂代谢(HDL)有关。

Objective To observe the characteristics of glucose, lipid and bone metabolism and bone mineral density (BMD)in postmenopausal women with type 2 diabetes mellitus (T2DM)in Shihezi district of Xinjiang province, and to investigate the relationship in the polymorphism and mutation of rs3736228 and rs3781586 of LRP5 gene and glucose,lipid and bone metabolism indexes in this population. Method A total of 136 postmenopausal Han women, who were related in the outpatient department, community, and hospital after hospitalization in Shihezi district of Xinjiang province from October 2016 to October 2017, were selected as the study subjects by the inclusion criteria and exclusion criteria.According to the patient's medicalhistory, glucosetolerance test results and bone mineral density (BMD), they were divided into 4 groups: normal glucose tolerance and normal bone mass (group A), normal glucose tolerance and abnormal bone mass (group B), type 2 diabetes and normal bone mass (group C), and type 2 diabetes mellitus and abnormal bone mass (group D). Baseline data such as patient's age, menopause years were measured and recorded, and body mass index (BMI)was calculated. Simultaneously, glucose metabolism indicators including fasting blood glucose (FBG, etc), bone metabolism indicators (blood Ca, etc), lipid metabolism indicators(triglycerides, etc)were detected. The polymorphisms of rs3736228 and rs3781586 of LRP5 gene were determined by Maldi-Tof-Ms and those data were analyzed statistically. Results ①Glucose metabolism index: compared with group A: FPG and HbAlc in group C, group D were all higher than group A (P<0.01). Lipid metabolism index: compared with group A, TG in group B and group D was lower than that in group A (P<0.05). Bone metabolism index: compared with group A, BMD (L1- 4)and BMD (femoral neck)in group B and group D were lower than those in group A (P<0.01). ②The distribution of SNP genotypes at rs3736228, rs3781586 of LRP5 conformsed to the Hardy-Weinberg genetic equilibrium law (P>0.05). The distribution frequency and allele frequency of LRP5 genotypes rs3736228, rs3781586 were compared among the groups. Pearson chi-square test showed no significant difference (P>0.05). ③Rs 3736228 locus of LRP5 gene:in group A, compared with CC (wild type), CT/TT (mutated type)triglyceride (TG)decreased (P<0.05), BMD (L1- 4)decreased (P<0.05). In group C, compared with CC (wild type), CT/TT (mutated type)high-density lipoprotein (HDL-C)increased (P<0.05), phosphorus increased (P<0.05). Rs 3781586 locus of LRP5 gene: in group B, compared with GG (wild type), GT/TT (mutated type)high-density lipoprotein (HDL-C)increased (P<0.05).Conclusion In the Xinjiang Shihezi district among postmenopausal women with type 2 diabetes, rs3736228, rs3781586 loci of LRP5 gene polymorphism may be irrelevant to glucose metabolism, but the mutation of rs3736228 of LRP5 gene locus may be related to lipid metabolism and bone metabolism (TG, HDL-C, BMD, P), and the mutation of rs3781586 may be related to lipid metabolism (HDL-C).

目的 探究m6A甲基化基因与卵巢癌生存预后的关系,为卵巢癌的靶向治疗、预后评估提供科学依据。方法 从TCGA及GTEx数据库中下载卵巢癌组织与正常组织mRNA表达数据进行组间差异分析,通过LASSO回归筛选与卵巢癌生存相关基因,进一步使用逐步Cox回归分析构建风险评分预测模型,根据风险评分中位数将患者分为高风险组和低风险组并使用ROC曲线下面积评价模型的预测能力。相关性分析构建与m6A基因的共表达调控网络,GO功能富集和KEGG通路分析初步探讨潜在的生物作用机制。结果 在癌组织与正常组织中发现20个m6A甲基化基因差异表达,逐步Cox回归分析筛选出3个基因(HNRNPA2B1,ZC3H13,WTAP)用于构建风险评分模型,高风险组患者的生存期较低风险组患者明显缩短(P=0.001 9),死亡风险显著增加(HR=2.643, P＜0.01),风险评分模型结合患者年龄、临床分级和分期后,1、3、5年的AUC为0.74、0.64、0.64。生物信息学分析结果提示m6A相关基因参与RNA的剪接、定位、转运、代谢调控、蛋白水解、细胞周期、核糖体合成等生物学过程。结论 成功构建卵巢癌m6A甲基化基因预后风险评估模型且该模型具备一定的预测效能。

Objective To explore the relationship between m6A methylated genes and prognosis of ovarian cancer, so as to provide scientific basis for targeted therapy and prognosis assessment of ovarian cancer. Methods The mRNA expression data of ovarian cancer tissues and normal tissues were downloaded from TCGA and GTEx databases for difference analysis between two groups. The genes related to ovarian cancer survival were screened by LASSO regression, and the risk score prediction model was further constructed by step Cox regression analysis. The patients were divided into high-risk group and low-risk group according to the median risk score, and the ROC was used for analysis. Correlation analysis was performed to construct an expression regulatory network with m6A genes, and GO function enrichment and KEGG pathway analysis were performed to preliminarily explore the potential biological mechanism. Results 20 m6A methylation genes were found in differential expression between cancer tissue and normal tissue, three genes (HNRNPA2B1, ZC3H13, WTAP) were used to construct the model through step Cox regression analysis. Patients' survivals of high-risk group were shortened than that of the low-risk group obviously (P=0.001 9), the risk of death significantly was increased (HR=2.643, P<0.01). After risk score model combined with patient age, clinical classification and stage, the AUC of 1, 3, 5 years was 0.74, 0.64 and 0.64. Bioinformatics analysis indicated that those m6A genes were involved in RNA splicing, localization, transport, metabolic regulation, proteolysis, cell cycle, ribosome synthesis and other biological processes. Conclusion The prognostic risk assessment model of m6A methylated genes for ovarian cancer was successfully constructed and the model had certain predictive efficacy.