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甲基转移酶样蛋白3在胃肠道肿瘤中参与有氧糖酵解的研究进展

马得原, 王娜, 王会强, 关泉林

马得原, 王娜, 王会强, 关泉林. 甲基转移酶样蛋白3在胃肠道肿瘤中参与有氧糖酵解的研究进展[J]. 肿瘤防治研究, 2024, 51(8): 697-702. DOI: 10.3971/j.issn.1000-8578.2024.24.0045
引用本文: 马得原, 王娜, 王会强, 关泉林. 甲基转移酶样蛋白3在胃肠道肿瘤中参与有氧糖酵解的研究进展[J]. 肿瘤防治研究, 2024, 51(8): 697-702. DOI: 10.3971/j.issn.1000-8578.2024.24.0045
MA Deyuan, WANG Na, WANG Huiqiang, GUAN Quanlin. Research Progress on Methyltransferase-like Protein 3 in Progression of Aerobic Glycolysis in Gastrointestinal Tumors[J]. Cancer Research on Prevention and Treatment, 2024, 51(8): 697-702. DOI: 10.3971/j.issn.1000-8578.2024.24.0045
Citation: MA Deyuan, WANG Na, WANG Huiqiang, GUAN Quanlin. Research Progress on Methyltransferase-like Protein 3 in Progression of Aerobic Glycolysis in Gastrointestinal Tumors[J]. Cancer Research on Prevention and Treatment, 2024, 51(8): 697-702. DOI: 10.3971/j.issn.1000-8578.2024.24.0045

甲基转移酶样蛋白3在胃肠道肿瘤中参与有氧糖酵解的研究进展

详细信息
    作者简介:

    马得原(1997-),男,硕士在读,主要从事胃癌基础与临床研究,ORCID: 0009-0007-7379-6440

    通讯作者:

    关泉林(1968-),男,博士,主任医师,主要从事肿瘤基础与临床研究,E-mail: guanql@lzu.edu.cn,ORCID: 0000-0003-0409-6823

  • 中图分类号: R735.3

Research Progress on Methyltransferase-like Protein 3 in Progression of Aerobic Glycolysis in Gastrointestinal Tumors

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  • 摘要:

    代谢重编程是恶性肿瘤发生发展的重要特征之一,为肿瘤提供了足够的能量和物质。在肿瘤细胞获得代谢重编程的过程中,表观遗传学的改变发挥了重要作用。 mRNA中的N6-腺苷甲基化(m6A)作为mRNA最常见的翻译后修饰途径,在mRNA的转录、成熟、翻译、降解等方面均发挥着调节作用。研究表明,m6A有助于推动肿瘤细胞的代谢重编程,但完整机制仍有待进一步研究。甲基转移酶样蛋白3(METTL3)作为m6A甲基化的关键酶,通过与其他蛋白质如METTL14、WTAP等形成m6A甲基转移酶复合物催化m6A,然而METTL3在胃肠道肿瘤糖代谢转变过程中的关键作用仍未得到重视。本文通过对METTL3在胃肠道肿瘤中影响细胞糖代谢重编程的具体途径进行总结,旨在阐明METTL3在胃肠道肿瘤能量重编程中的重要性。

     

    Abstract:

    Metabolic reprogramming is one of the significant characteristics of malignant tumor development. It provides the tumor with sufficient energy and materials. During the process by which tumor cells acquire metabolic reprogramming, epigenetic changes play a crucial role. N6-methyladenosine (m6A) in mRNA is the most common post-transcriptional modification of mRNA. It regulates the transcription, maturation, translation, and degradation of mRNA. Studies have shown that m6A helps promote the metabolic reprogramming of tumor cells. However, the complete mechanism still requires further research. METTL3 is a key enzyme for m6A methylation that catalyzes m6A progression by forming complexes with other proteins, such as METTL14 and WTAP. Notably, the critical role of METTL3 in the metabolic transition of gastrointestinal tumors has not been given due attention. This article summarizes the specific pathways through which METTL3 affects the reprogramming of cellular glucose metabolism in gastrointestinal tumors. We aimed to clarify the importance of METTL3 in the energy reprogramming of gastrointestinal tumors.

     

  • 男性乳腺癌在临床中比较罕见,发病率占所有乳腺癌的0.9%~1.4%[1-4]。近年来,男性乳腺癌的发病率呈上升趋势,并有研究显示,男性乳腺癌的发病率和死亡率在地区之间存在差异[5]。男性乳腺癌在就诊时多分期较晚,且恶性程度较高,预后较女性乳腺癌差[6-7]。由于其发病率低,目前针对于男性乳腺癌的诊断和治疗标准均参照女性乳腺癌,而这些诊治标准可能并不完全适用于男性乳腺癌患者。现有的文献中男性乳腺癌个例和小样本研究比较普遍,缺乏大样本的研究,因此,有必要对男性乳腺癌进行系统的研究和分析,包括流行病学特征、预防、诊断、治疗和预后。本文对2012—2015年湖北省男性乳腺癌的发病率和死亡率进行分析,预测其发病及死亡规律,为湖北省乃至全国乳腺癌防控策略制定可靠的科学依据。

    本研究数据来源于2012—2015年湖北省肿瘤登记处上报的乳腺癌发病、死亡及人口数据。2012—2015年分别上报了7、9、13和16个肿瘤登记处的数据,分别占全省人口总数的14%、18%、23%和27%。包含地级以上城市(城市地区)和县及县级市(农村地区),提取信息包括性别、地区、年龄别(采用《中国肿瘤登记年报》中年龄别的界定)、发病率和死亡率等。

    根据《中国肿瘤登记工作指导手册》,并按照国际癌症研究中心(International Agency for Research on Cancer, IARC)/国际癌症登记协会(International Association for Cryptologic Research, IACR)对登记质量的有关要求,对湖北省登记地区2012—2015年的原始数据进行审核和评估,病理学诊断比例(morphological verification percentage, MV%)、仅有死亡医学证明书比例(DCO%)和死亡发病比(M/I)是评价登记资料完整性和有效性的重要指标。如在审核过程中发现质量问题,及时反馈给各登记处,并对重新提交的资料进行复审直至符合相应标准。本研究资料中2012—2015年湖北省肿瘤登记处MV%达标率分别为86%、100%、100%和100%,符合MV%为55%~95%的质量登记要求;平均DCO%分别为0.45%、1.59%、0.41%和0.42%,也基本上符合国家0~10%肿瘤登记质量要求;4年间各肿瘤登记点分别有4、6、8和14个M/I值,均达到国家肿瘤质量要求(0.6~0.8),少数M/I值偏低。

    应用GRAPH PAD 8.0.2软件进行原始数据分析。分组因素包含城乡及年龄别(0、1~4、5~9、10~14、15~19...、85+)。组间差异仅对数据大小进行描述和对比,未进行P值的计算。

    共累计覆盖48 010 069人,2012—2015年分别覆盖8 221 036、10 439 769、13 338 644和16 010 620人,其中男性24 502 475人,女性23 507 594人。肿瘤登记处地区分为城市地区(地级以上城市)和农村地区(县和县级市),城市地区包含武汉市和宜昌市,农村地区包含公安县、五峰县、麻城市、云梦县、钟祥市、嘉鱼县、洪湖市、京山县、恩施市、宜城市、郧阳区、大冶市、通城县和天门市等多个地区,具体信息见表 1

    表  1  2012—2015年湖北省肿瘤登记处上报的地区分布和人口数据
    Table  1  Regional distribution and population data reported by Hubei Cancer Registry from 2012 to 2015
    下载: 导出CSV 
    | 显示表格

    共报告106例新发男性乳腺癌,新发女性乳腺癌10 052例。男性和女性乳腺癌发病率分别为0.43/105和42.76/105,男女发病率比为1:99,见图 1。男性乳腺癌发病率不同年份间差异并不明显,男女性乳腺癌发病率占比均接近1:100。城市和农村地区男性乳腺癌发病率互有高低,并无明显差异,见表 2

    图  1  2012—2015年湖北省男性和女性乳腺癌累计发病率(A)和死亡率(B)占比
    Figure  1  Percentage of cumulative incidence(A) and mortality(B) of male and female breast cancer in Hubei Province from 2012 to 2015
    表  2  2012—2015年湖北省乳腺癌发病率
    Table  2  Incidence of breast cancer in Hubei Province from 2012 to 2015
    下载: 导出CSV 
    | 显示表格

    2012—2015年湖北省男性乳腺癌在0~34岁阶段发病率极低,34岁以后总体发病率随着年龄增加而上升,54岁以后呈交叉上升趋势,于85岁以上达到峰值。城市和农村地区总体年龄别发病率变化趋势与全部男性乳腺癌基本保持一致,城市和农村地区在不同年龄区间发病率互有高低,城市地区发病率峰值同样位于85岁以上,农村地区则为75~79岁,见图 2

    图  2  2012—2015年湖北省男性乳腺癌累计年龄别发病率分布情况
    Figure  2  Cumulative age-specific incidence of male breast cancer in Hubei Province from 2012 to 2015

    2012—2015年湖北省城市和农村地区男性乳腺癌总体发病率并无显著差异,4年间城市地区男性乳腺癌平均发病率为0.40/105,农村地区为0.47/105,农村地区略高于城市地区。不同年份男性乳腺癌发病率互有高低,2012和2015年城市和农村地区发病率基本一致,2013年城市地区高于农村地区,2014年农村地区远高于城市地区,见表 2图 3

    图  3  2012—2015年湖北省城市和农村地区累计男性乳腺癌发病率分布情况
    Figure  3  Cumulative incidence of male breast cancer in urban and rural areas in Hubei Province from 2012 to 2015

    共报告37例男性乳腺癌死亡病例,2 201例女性乳腺癌死亡病例。男性和女性乳腺癌死亡率分别为0.15/105和9.36/105,男女死亡率比为1:62,见图 1。不同年份间男性乳腺癌死亡率差异较大,男女性乳腺癌死亡率占比为1:45到1:88。城市和农村地区男性乳腺癌死亡率互有高低,见表 3图 4

    表  3  2012—2015年湖北省乳腺癌死亡率
    Table  3  Mortality of breast cancer in Hubei Province from 2012 to 2015
    下载: 导出CSV 
    | 显示表格
    图  4  2012—2015年湖北省男性乳腺癌累计年龄别死亡率分布情况
    Figure  4  Cumulative age-specific mortality of male breast cancer in Hubei Province from 2012 to 2015

    2012—2015年湖北省男性乳腺癌在0~44岁阶段死亡率极低,44~69岁阶段死亡率随着年龄增加而上升,70~74岁年龄段下降后急剧上升,85岁以上达到峰值。城市和农村地区的年龄别死亡率差距不大,城市和农村地区总体年龄别死亡率变化趋势与全部男性乳腺癌基本保持一致,在不同年龄区间互有高低,城市地区和农村地区发病率峰值同样在85岁以上,见图 4

    2012—2015年湖北省城市和农村地区男性乳腺癌总体死亡率无差异,4年间城市地区和农村地区平均死亡率均为0.16/105。不同年份城市和农村地区男性乳腺癌死亡率互有高低,2012和2014年城市地区死亡率低于农村地区,2013和2015年城市地区死亡率高于农村地区,见表 3图 5

    图  5  2012—2015年湖北省城市和农村地区累计男性乳腺癌死亡率分布情况
    Figure  5  Cumulative mortality of male breast cancer in urban and rural areas in Hubei Province from 2012 to 2015

    男性乳腺癌虽然发病率较低,但在过去几十年间,男性乳腺癌的发病率呈明显的上升趋势[8-9]。本研究中男女发病率比例为1:99,与其他临床研究结果接近[1-4]。女性乳腺癌的发病率随着年龄上升而上升。相关临床数据显示,男性乳腺癌发病率也随年龄增长而升高。本研究结果显示男性乳腺癌发病率到85岁以上时达到峰值,国内其他研究男性乳腺癌发病率峰值为71岁。因地区不同也存在很大的差距,非洲男性发病率最高,其次为北美洲及欧洲,亚洲最低[5]。本研究中城市地区和农村地区男性乳腺癌发病率无明显差异。

    随着乳腺癌精准治疗的意识普及及男性乳腺癌发病率的升高,男性乳腺癌也逐渐引起了社会的关注,但仍有大部分的男性乳腺癌在发现时分期较晚、恶性程度较高[7],再加上对男性乳腺癌的认识不足,缺乏特定的治疗手段,不能做出最恰当的治疗决策,导致了男性乳腺癌预后较差[10]。美国NCDB(National Cancer Database)数据库对2004—2014年的数据进行统计及分析,发现10年间男性乳腺癌的死亡率有下降的趋势,但同时期内男性乳腺癌死亡率(27.2%)仍显著高于女性乳腺癌(17.4%)。女性乳腺癌5年和10年生存率分别为85%和71%,而男性乳腺癌分别为75%和56%。女性患者的中位生存期为13.2年,男性为11.4年。这些均提示了男性乳腺癌较差的预后[11-12]。目前全球尚无男性乳腺癌的临床规范治疗指南及大型临床研究,因而,男性乳腺癌的治疗大部分参照了女性乳腺癌的治疗标准进行,尤其是绝经后女性乳腺癌,即使男性乳腺癌与绝经后女性体内激素环境相似,但在本质上存在差异[10-12],完全沿用女性乳腺癌相关的临床指南来指导男性乳腺癌的治疗,存在较大的隐患,女性乳腺癌的治疗在近几十年取得了较大进展,特别是在药物研究方面取得了大突破,如靶向治疗、内分泌治疗及免疫治疗方面,而针对男性乳腺癌的研究也需要进一步得到关注和实施,以此来提升男性乳腺癌的治疗效果。本研究中男女性乳腺癌发病率之比为1:99,而死亡率之比为1:62,也同样提示男性乳腺癌较差的预后。男性乳腺癌死亡率为0.15/105,34岁以后男性乳腺癌死亡率随着年龄增长而迅速上升,85岁以上时达到峰值。2012—2015年不同年份间的城乡地区的死亡率互有高低。但由于目前湖北省肿瘤登记点还不完善,人口普及度也有待提高,男性乳腺癌数据相对较少,对于其发病率和死亡率的结论可靠性不足,需要更多的数据来进行系统性分析。

    随着社会经济的高速发展,医疗水平也高速发展,乳腺癌的筛查越来越普遍,并且因为社会发展带来的人口老龄化问题、平均寿命增加、饮食、环境及辐射等各种内外因素的影响,无论是男性或者女性乳腺癌发病率都呈现逐年上升的趋势,男性乳腺癌发病率增速甚至超过了女性乳腺癌,在美国每年有约2 000例新发男性乳腺癌患者[13],研究显示,1975—2015年,美国男性乳腺癌发病率上升了40%,比女性乳腺癌高25%[9]。男性乳腺癌发病率随着年龄的增长而逐渐上升,地区间也存在差异,可能与地区之间经济发展差异、种族、医疗水平、饮食、生活习惯及环境等都存在相关性。男女性乳腺癌间存在差异,因而,需要对男性乳腺癌的相关数据进行收集和分析,得出相关的流行病学数据及临床诊疗数据。此外,还需要针对男性乳腺癌患者开展相关临床研究,制定出针对男性乳腺癌患者的诊疗指南,才符合乳腺癌精准治疗的趋势。

    随着乳腺癌精准化治疗的推进,男性乳腺癌也应受到社会各级单位的重视,需要加大对男性乳腺癌的研究及相关指南的制定,各级单位应向群众普及男性乳腺癌的发病及死亡率等流行病学知识,研究男性乳腺癌的临床特征及诊治手段,加强对医护人员的知识培训,提升医护人员和群众对男性乳腺癌的认识,加强疾病的早筛早治,以此改善男性乳腺癌的预后。

    Competing interests: The authors declare that they have no competing interests.
    利益冲突声明:
    所有作者均声明不存在利益冲突。
    作者贡献:
    马得原:文献查阅、论文撰写
    王 娜:思路设计、归类总结
    王会强:资料整理、数据分析
    关泉林:论文修改及审阅
  • 表  1   METTL3对糖酵解相关蛋白的影响途径汇总

    Table  1   Summary of pathways of METTL3 affecting glycolysis-related proteins

    ProteinTumor
    model
    Modification
    site
    EffectResult
    GLUT1CRC3′UTREnhance the affinity of IGF2BP2/3 for m6A sitesEnhanced stability and expression
    levels of mRNA
    GLUT1CRCSOX2 mRNA CDSEnhance the affinity of IGF2BP3 for m6A sites and
    activation of SOX2-lncRNA AC005392.2-GLUT1 axis
    Ubiquitinates GLUT1 and inhibits
    its degradation
    HK2
    CRC5′/3′UTREnhance the affinity of IGF2BP2 for m6A sitesEnhanced stability and expression
    levels of mRNA
    LDHACRCCDSEnhance the affinity of YTHDF1 for m6A sitesEnhanced translation of LDHA
    G6PDCRCLINC01615Inhibition of the interaction between hnRNPA1
    and G6PD pre-mRNA
    Improved the splicing efficiency
    of G6PD pre-mRNA
    PGAM1CRCcircQSOX1Adsorption of miR-326/miR-330-5pElevated levels of PGAM1
    NDUFA4GC3′UTREnhance the affinity of IGF2BP1 for m6A sitesEnhanced stability and expression
    levels of mRNA
    Notes: CRC: colorectal cancer; GC: gastric cancer.
    下载: 导出CSV

    表  2   METTL3对糖酵解相关信号通路的影响途径

    Table  2   Pathways of METTL3 affecting glycolysis-related signaling pathways

    Tumor
    model
    Modified
    regulatory sites
    Signaling pathway
    GC pri-miR-17-92 PTEN/PI3K/AKT
    CRC LINC01559 miR-106-5p/PTEN/PI3K/AKT
    CRC EphA2 and VEGFA PI3K/AKT/mTOR
    GC KRT18 MAPK/ERK
    CRC pri-miR-1246 SPRED2/MAPK
    CRC Sec62 Wnt/β-catenin
    CRC REG1α Wnt/β-catenin
    下载: 导出CSV

    表  3   METTL3通过影响转录因子调控糖酵解相关蛋白的表达

    Table  3   Regulation of glycolytic protein expression by METTL3 through transcription-factor modulation

    Transcription factor Tumor model Effector pathway Downstream effector protein
    HDGF GC Nuclear HDGF binds to the promoters of GLUT4 and ENO2. GLUT4, ENO2
    HIF-1α GC,CRC HIF-1α binds to the hypoxia response element (HRE)
    in the promoter region.
    METTL3, GLUT1, GLUT3, etc.
    HIF-1α CRC HIF-1α elevates mRNA levels and activates the promoter. LDHA
    P53 GC - GLUT1, GLUT3, GLUT4
    Note: -: no data.
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  • 收稿日期:  2024-01-16
  • 修回日期:  2024-05-06
  • 刊出日期:  2024-08-24

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