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Article(id=1207314219796631688, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1207314214872518754, articleNumber=null, orderNo=null, doi=10.14109/j.cnki.xyylc.2025.04.03, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1690128000000, receivedDateStr=2023-07-24, revisedDate=null, revisedDateStr=null, acceptedDate=1733068800000, acceptedDateStr=2024-12-02, onlineDate=1765775740813, onlineDateStr=2025-12-15, pubDate=1745510400000, pubDateStr=2025-04-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1765775740813, onlineIssueDateStr=2025-12-15, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1765775740813, creator=13701087609, updateTime=1765775740813, updator=13701087609, issue=Issue{id=1207314214872518754, tenantId=1146029695717560320, journalId=1205117082300743687, year='2025', volume='44', issue='4', pageStart='241', pageEnd='320', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=0, createTime=1765775739638, creator=13701087609, updateTime=1765775882010, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1207314812124635584, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1207314214872518754, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1207314812124635585, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1207314214872518754, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=252, endPage=257, ext={EN=ArticleExt(id=1207314220132176027, articleId=1207314219796631688, tenantId=1146029695717560320, journalId=1205117082300743687, language=EN, title=Research progress on treatment of hepatocellular carcinoma in m6A methylated modification, columnId=1207314219599499390, journalTitle=Chinese Journal of New Drugs and Clinical Remedies, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

N6-methyladenosine（m6A） methylation is involved in the whole process of mRNA biological behavior and plays an important role in the malignant progression of cancer. This article reviewed the invasion and metastasis of m6A methylation in hepatocellular carcinoma （HCC）, its regulation with non-coding RNA, and the effect of immunotherapy. It is very important to find that m6A methylated regulatory proteins are involved in the development and prognosis of HCC.m6A methylation is closely related to the regulation of non-coding RNA on the proliferation, metastasis and drug resistance of HCC. In terms of immunotherapy, circRHBDD1 and BTBD10 participate in m6A methylation modification to regulate cell metabolism and inhibit the immune escape of cancer cells, which can be used for the HCC diagnosis and innovative drug discovery in the future.

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N6-甲基腺苷（m6A）甲基化修饰参与mRNA生物学行为的全过程，在癌症的恶性进展中发挥了重要作用。本文对m6A甲基化修饰在肝细胞癌（HCC）的侵袭、发生、发展与转移中的作用，以及与非编码RNA之间的调控、免疫治疗作用进行综述。有关HCC的m6A甲基化修饰的调控蛋白，在HCC的发生、发展、转移以及预后是至关重要的；m6A甲基化修饰调节与非编码RNA之间的互相调控，与HCC的增殖、转移以及耐药性密切相关；在免疫治疗方面，最新发现的circRHBDD1与BTBD10参与m6A甲基化修饰调控的细胞代谢，抑制肿瘤细胞的免疫逃逸，该领域的研究可用于未来HCC的诊断与创新药物发现。

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史晶晶，女，副教授，硕士，主要从事中药药理学研究，E-mail:

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史晶晶，女，副教授，硕士，主要从事中药药理学研究，E-mail:

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史晶晶，女，副教授，硕士，主要从事中药药理学研究，E-mail:

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非编码RNA种类非编码RNA变化情况m6A甲基化靶点作用机制功能文献
miRNAmiR-126表达升高METTL14抑制METTL14抑制HCC细胞转移［24］
miR-145表达升高YTHDF2通过调节YTHDF2的mRNA3’-UTR，下调YTHDF2的过表达抑制HCC细胞的增殖［25］
circRNAcircMEG3表达升高METTL3circMEG3通过METTL3抑制端粒合成酶H/ACA核糖核蛋白（Cbf5）的表达抑制HCC干细胞恶性分化［26］
circDLC1表达升高KIAA1429KIAA1429的沉默能增加circDLC1表达，促进肝癌细胞增殖与转移抑制HCC细胞的生长与转移细胞［27］
circRHBDD1表达升高YTHDF1circRHBDD1将YTHDF1招募到PIK3R1 mRNA并加速PIK3R1的翻译，增强有氧糖酵解限制了HCC中的抗PD-1的耐药性［28］
circGPR137B表达升高FTOcircGPR137B通过circGPR137B/miR-4739/FTO反馈回路抑制HCC肿瘤发生和转移抑制HCC肿瘤发生和转移［29］
lncRNALINC00958表达升高METTL3METTL3增加了LINC00958的稳定性，抑制miR-3619-5p的表达，升高HDGF表达促进HCC的生成［30］
LNCAROD表达升高METTL3、IGF2BP3在细胞质中竞争性地与miR-145-5p结合，上调PKM2表达，增强有氧糖酵解促进HCC进展和化疗药物的耐药性［31］
LINC00106表达升高METTL3、IGF2BP1竞争结合海绵let7f，并影响PI3K-Akt信号通路增强HCC的干细胞特性和转移性［32］
LINC01273表达升高METTL3、YTHDF2LINC01273促进miR-600的稳定性，增强miR-600对METTL3的抑制作用，导致METTL3表达降低促进HCC细胞对索拉非尼耐药［33］
NIFK-AS1表达升高METTL3、IGF2BP1METTL3/IGF2BP1轴可以提高NIFK-AS1 RNA的稳定性，增加NIFK-AS1的表达，并影响miR-637/AKT1/MMP-7和MMP-9轴。转运体OATP1B1/OATP1B3对索拉非尼的摄取和转运减少促进HCC细胞对索拉非尼耐药［34］
DUXAP8表达升高METTL3METTL3促进DUXAP8的稳定性，竞争性结合miR-584-5p激活靶基因MAPK1和MAPK-ERK信号通路促进HCC进展和干细胞特性［35］
ILF3-AS1表达升高METTL3、GF2BP1METTL3/IGF2BP1提高ILF3-AS1的稳定性，升高NIFK-AS1表达促进HCC细胞增殖、迁移和侵袭［36］
LncAY表达升高YTHDF2YTHDF2增加LncCY的半衰期，促进BMI1的表达，激活Wnt/b-catenin信号通路促进HCC细胞增殖和迁移［37］
MEG3表达降低METTL3通过ceRNA机制，促进miR-544b表达，降低靶基因BTG2表达抑制HCC细胞增殖、侵袭和迁移［38］
), ArticleFig(id=1207314226415243653, tenantId=1146029695717560320, journalId=1205117082300743687, articleId=1207314219796631688, language=CN, label=表1, caption=

非编码RNA与m6A甲基化修饰相互调控参与肝细胞癌（HCC）

, figureFileSmall=null, figureFileBig=null, tableContent=
非编码RNA种类非编码RNA变化情况m6A甲基化靶点作用机制功能文献
miRNAmiR-126表达升高METTL14抑制METTL14抑制HCC细胞转移［24］
miR-145表达升高YTHDF2通过调节YTHDF2的mRNA3’-UTR，下调YTHDF2的过表达抑制HCC细胞的增殖［25］
circRNAcircMEG3表达升高METTL3circMEG3通过METTL3抑制端粒合成酶H/ACA核糖核蛋白（Cbf5）的表达抑制HCC干细胞恶性分化［26］
circDLC1表达升高KIAA1429KIAA1429的沉默能增加circDLC1表达，促进肝癌细胞增殖与转移抑制HCC细胞的生长与转移细胞［27］
circRHBDD1表达升高YTHDF1circRHBDD1将YTHDF1招募到PIK3R1 mRNA并加速PIK3R1的翻译，增强有氧糖酵解限制了HCC中的抗PD-1的耐药性［28］
circGPR137B表达升高FTOcircGPR137B通过circGPR137B/miR-4739/FTO反馈回路抑制HCC肿瘤发生和转移抑制HCC肿瘤发生和转移［29］
lncRNALINC00958表达升高METTL3METTL3增加了LINC00958的稳定性，抑制miR-3619-5p的表达，升高HDGF表达促进HCC的生成［30］
LNCAROD表达升高METTL3、IGF2BP3在细胞质中竞争性地与miR-145-5p结合，上调PKM2表达，增强有氧糖酵解促进HCC进展和化疗药物的耐药性［31］
LINC00106表达升高METTL3、IGF2BP1竞争结合海绵let7f，并影响PI3K-Akt信号通路增强HCC的干细胞特性和转移性［32］
LINC01273表达升高METTL3、YTHDF2LINC01273促进miR-600的稳定性，增强miR-600对METTL3的抑制作用，导致METTL3表达降低促进HCC细胞对索拉非尼耐药［33］
NIFK-AS1表达升高METTL3、IGF2BP1METTL3/IGF2BP1轴可以提高NIFK-AS1 RNA的稳定性，增加NIFK-AS1的表达，并影响miR-637/AKT1/MMP-7和MMP-9轴。转运体OATP1B1/OATP1B3对索拉非尼的摄取和转运减少促进HCC细胞对索拉非尼耐药［34］
DUXAP8表达升高METTL3METTL3促进DUXAP8的稳定性，竞争性结合miR-584-5p激活靶基因MAPK1和MAPK-ERK信号通路促进HCC进展和干细胞特性［35］
ILF3-AS1表达升高METTL3、GF2BP1METTL3/IGF2BP1提高ILF3-AS1的稳定性，升高NIFK-AS1表达促进HCC细胞增殖、迁移和侵袭［36］
LncAY表达升高YTHDF2YTHDF2增加LncCY的半衰期，促进BMI1的表达，激活Wnt/b-catenin信号通路促进HCC细胞增殖和迁移［37］
MEG3表达降低METTL3通过ceRNA机制，促进miR-544b表达，降低靶基因BTG2表达抑制HCC细胞增殖、侵袭和迁移［38］
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m6A甲基化修饰在肝细胞癌治疗中的作用研究进展
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史晶晶 , 时博 , 王小兰
中国新药与临床杂志 | 综述 2025,44(4): 252-257
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中国新药与临床杂志 | 综述 2025, 44(4): 252-257
m6A甲基化修饰在肝细胞癌治疗中的作用研究进展
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史晶晶 , 时博, 王小兰
作者信息
  • 河南中医药大学，河南　郑州　450046

    • 史晶晶，女，副教授，硕士，主要从事中药药理学研究，E-mail:

Research progress on treatment of hepatocellular carcinoma in m6A methylated modification
Jing-jing SHI , Bo SHI, Xiao-lan WANG
Affiliations
  • Henan University of Chinese Medicine, Zhengzhou HE-NAN 450046, China
出版时间: 2025-04-25 doi: 10.14109/j.cnki.xyylc.2025.04.03
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摘要
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N6-甲基腺苷（m6A）甲基化修饰参与mRNA生物学行为的全过程，在癌症的恶性进展中发挥了重要作用。本文对m6A甲基化修饰在肝细胞癌（HCC）的侵袭、发生、发展与转移中的作用，以及与非编码RNA之间的调控、免疫治疗作用进行综述。有关HCC的m6A甲基化修饰的调控蛋白，在HCC的发生、发展、转移以及预后是至关重要的；m6A甲基化修饰调节与非编码RNA之间的互相调控，与HCC的增殖、转移以及耐药性密切相关；在免疫治疗方面，最新发现的circRHBDD1与BTBD10参与m6A甲基化修饰调控的细胞代谢，抑制肿瘤细胞的免疫逃逸，该领域的研究可用于未来HCC的诊断与创新药物发现。

m6A甲基化修饰  /  肝细胞癌  /  非编码RNA  /  免疫治疗  /  circRHBDD1  /  BTBD10

N6-methyladenosine（m6A） methylation is involved in the whole process of mRNA biological behavior and plays an important role in the malignant progression of cancer. This article reviewed the invasion and metastasis of m6A methylation in hepatocellular carcinoma （HCC）, its regulation with non-coding RNA, and the effect of immunotherapy. It is very important to find that m6A methylated regulatory proteins are involved in the development and prognosis of HCC.m6A methylation is closely related to the regulation of non-coding RNA on the proliferation, metastasis and drug resistance of HCC. In terms of immunotherapy, circRHBDD1 and BTBD10 participate in m6A methylation modification to regulate cell metabolism and inhibit the immune escape of cancer cells, which can be used for the HCC diagnosis and innovative drug discovery in the future.

m6A methylated modification  /  hepatocellular carcinoma  /  non-coding RNA  /  immunotherapy  /  circRHBDD1  /  BTBD10
史晶晶, 时博, 王小兰. m6A甲基化修饰在肝细胞癌治疗中的作用研究进展. 中国新药与临床杂志, 2025 , 44 (4) : 252 -257 . DOI: 10.14109/j.cnki.xyylc.2025.04.03
Jing-jing SHI, Bo SHI, Xiao-lan WANG. Research progress on treatment of hepatocellular carcinoma in m6A methylated modification[J]. Chinese Journal of New Drugs and Clinical Remedies, 2025 , 44 (4) : 252 -257 . DOI: 10.14109/j.cnki.xyylc.2025.04.03
正文
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肝细胞癌（hepatocellular carcinoma，HCC）是最常见的具有侵略性的恶性肿瘤之一。据统计，2020年全世界HCC新发病例约84.1万人，死亡病例78.2万人；我国是HCC高发国家，死亡病例占了世界死亡病例的一半以上[1]，2022年调查统计研究显示，我国女性老年人群HCC发病率与死亡率高达60%以上，远高于美国、韩国、日本[2]。肝炎病毒感染、酒精肝、脂肪肝、黄曲霉素等是导致HCC的主要因素[3]，预后差主要是由于复发和转移。近年来，尽管在早期检测和临床治疗策略方面有所提高，但是对于晚期和化疗药物不敏感的HCC患者，生存率依然较低[4, 5]。N6-甲基腺苷（N6-methyladenosine，m6A）修饰在HCC发生与发展中的重要性日益被人们认识。研究表明，m6A甲基化在HCC的恶性进展、免疫治疗、非编码RNA调控方面发挥了重要作用[6, 7]。本文将m6A甲基化在HCC的发生、发展以及调控途径和免疫治疗方面进行综合阐述与分析，以期为寻找HCC的治疗新途径和靶点提供参考依据。
m6A甲基化修饰与HCC发生、发展的相关性
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m6A修饰是真核生物信使RNA（messenger RNA，mRNA）中最常见的修饰之一，几乎参与mRNA生物学行为的全过程，包括mRNA剪切、从细胞核向细胞质输出以及翻译起始、延伸和降解等[8]，是近年来生命科学领域的研究热点。
m6A甲基化修饰标志物包括甲基化转移酶、去甲基化酶、甲基化阅读蛋白等。其中甲基化转移酶包括METTL3/14、WTAP、KIAA1429等，主要作用就是催化mRNA上腺苷酸发生m6A修饰；去甲基化酶包括FTO、ALKBH5等，作用是对已发生m6A修饰的碱基进行去甲基化修饰；阅读蛋白包括YTHDF、IGF2BP等，主要功能是识别发生m6A修饰的碱基，从而激活下游的调控通路如RNA降解、miRNA加工等。RNA m6A修饰是利用m6A酶系统修饰靶向基因，导致靶向基因mRNA翻译改变，从而使原癌基因和抑癌基因表达改变，加速肿瘤发生和进展[9]。
1　m6A甲基化转移酶METTL14对HCC的调控
研究表明，m6A 甲基化及其相关蛋白在HCC的恶性进展中发挥了重要作用。LI等[10]通过挖掘TCGA数据库中的307例患者和GEO数据库中的64例患者发现，METTL14作为RNA m6A甲基化调控因子，通过调节半胱氨酸亚磺酸脱羧酶（cysteine sulfinic acid decarboxylase，CSAD）、谷氨酰胺-草酰乙酸转氨酶（glutamine-oxaloacetic transaminase，GOT）、细胞因子信号转导抑制因子2（suppressor of cytokine signaling 2，SOCS2），参与HCC的恶性进展。一项研究在男女各20例HCC样本中利用实时荧光定量核酸扩增检测的方法检测METTL14表达，发现其在HCC中表达降低，从而能够促进细胞凋亡、抑制细胞周期进程和细胞增殖，并且发现miR-126为METTL14靶基因，因此提出了METTL14与miRNA信号通路的相互作用理论模式，为治疗HCC的新思路[11]。时隔一年的另一项研究发现，METTL14表达在HCC中没有显著降低，还证实了METTL14对HCC细胞增殖和迁移的促进作用[12]。因此，有学者研究了METTL14对HCC细胞迁移能力影响的矛盾表现，发现可能是由细胞系的差异、METTL3/ METTL14杂合物的多功能性以及m6A独立模式造成的[13]，因此m6A修饰和m6A调控子在HCC发展中具有一定的异质性和复杂性。
2　m6A甲基化转移酶METTL3对HCC的调控
在HCC生发展中，上皮间质转化（epithelial mesenchymaltran-sition，EMT）参与机体多个生理病理过程，尤其与肿瘤侵袭与转移相关[14]。METTL3对于EMT是非常重要的，LIN等[15]发现在EMT中整体m6A mRNA表达显著升高，而体内外实验结果显示METTL3缺失会抑制HCC细胞侵袭、转移和EMT；METTL3与YTHDF1协同作用，促进EMT的关键转录因子Snail的翻译，这些发现解释了METTL3的过表达是如何导致HCC转移的。
桥粒相关蛋白Pinin通过与METTL3相互作用增加RNA的 m6A修饰水平，进而诱导Snail表达，表明Pinin通过调节m6A修饰诱导EMT，因此可能是HCC治疗的潜在抗癌靶点[16]。另外，在微波消融治疗HCC技术中，METTL3在46 ℃下诱导并触发HCC细胞中CD47的表达，而且CD47 mRNA降解对m6A的阅读蛋白IGF2BP1呈依赖性稳定，METTL3/IGF2BP1/CD47介导的EMT转变有助于HCC细胞中不完全消融诱导的转移，为微波消融治疗HCC的潜在靶点[17]。
另外，除了EMT参与的METTL3调控HCC侵袭与转移，也有研究显示，SOCS2为METTL3介导的靶基因，可以通过阅读蛋白YTHDF2途径降解，影响HCC 细胞增殖、迁移和集落形成，该发现为HCC发生中表观遗传改变的重要机制之一[18]。
3　m6A阅读蛋白YTHDF2对HCC的调控
m6A甲基化修饰阅读蛋白核YTH家族蛋白YTHDF1-3与核成员YTHDC1可以直接与包含m6A结构的RNA相结合，YTHDC1可以作为招募者，将原癌基因SRSF3带到m6A附近的mRNA结合区域，影响mRNA的稳定性，从而调控基因表达[19]。
YTHDF2在HCC组织中的表达明显升高，WANG等[20]采用免疫组化与组织芯片手段对40对HCC组织与癌旁组织样本进行检测，发现YTHDF2在HCC组织中的蛋白表达明显高于癌旁肝组织，同时通过GEPLA数据库分析验证，YTHDF2在HCC不同分期中均高表达，并在TIMER数据库分析得出YTHDF2的表达与HCC免疫微环境中各类免疫细胞呈正相关，对患者生存与预后均有不良影响。另外，YTHDF2 可以调控参与炎症介导、肿瘤恶化的2种因子——白细胞介素11（IL-11）和丝氨酸蛋白酶抑制剂（SERPINE2），从而加剧炎症和血管异常，形成恶性肿瘤[21]；并且与转录因子OCT4表达和OCT4 mRNA 5'-UTR中的m6A水平呈正相关，通过调节OCT4 mRNA的m6A甲基化水平来增加HCC中肿瘤干细胞表型高表达，促进肿瘤细胞转移[22]。
在低氧诱导的环境下，HCC中YTHDF2的表达降低，通过YTHDF2的过表达，可以抑制HCC的细胞增殖、肿瘤生长以及丝裂原活化蛋白激酶（mitogen-activated protein kinase，MAPK）和细胞外信号调节激酶（extracellular regulated protein kinases，ERK）的激活，这可能是因为YTHDF2可以结合表皮生长因子受体（epidermal growth factor receptor，EGFR） 3'-UTR的m6A修饰位点，以促进HCC细胞中EGFR mRNA的降解，从而通过使HCC中的EGFR mRNA表达不稳定来抑制肿瘤的增殖和生长[23]，因此，YTHDF2可能对HCC是一种双向调节的靶基因。
综上所述，m6A 甲基化修饰在HCC的侵袭转移中发挥了重要作用，其中甲基化转移酶（METTL3与METTL14）与阅读蛋白（YTHDF2与IGF2BP）为HCC研究的热点，可成为目前新兴抗癌药物的新型靶点，而去甲基化酶（FTO、ALKBH5）则相关研究较少，有待研究人员进一步的探索。
非编码RNA调控m6A甲基化修饰参与HCC的进程
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许多研究表明，发生m6A甲基化的非编码RNA在基因调控、干细胞分化、肿瘤细胞增殖、组织生长发育等过程中起关键作用。m6A作为真核细胞最丰富的修饰，其在HCC中相关的miRNA、lncRNA与circRNA调控和功能中的作用非常重要，在体外影响肿瘤细胞的生长、迁移与集落形成，在体内影响致瘤性、肿瘤组织的生长、肺转移以及耐药性，见表1。
非编RNA参与调控m6A甲基化的研究成果虽然有部分积累，但总结性较少，规律性不强。由表1可知，miRNA与circRNA的m6A甲基化研究较少，miRNA大部分是以lncRNA与circRNA海绵的形式调控HCC的发生发展，lncRNA的m6A甲基化在HCC中的耐药性和转移更为显著，而circGPR137B/miR-4739/FTO反馈回路是新型的正反馈机制，为表观遗传学提供了新模型，为治疗提供了新的参考和研究思路。
m6A甲基化修饰在HCC免疫治疗中的作用
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免疫检查点抑制剂的发现已经彻底改变了HCC的治疗方式，抗程序性死亡受体1（PD-1）治疗可以调节T细胞的杀伤活性，激活抗肿瘤免疫反应[39]。在一部分HCC患者中，虽然抗PD-1药物作用较为持久，但是也出现耐药性，整体阻断率较低的情况[40]。RNA m6A修饰通过YTHDF1调控肿瘤抗原特异性免疫反应，通过树突状细胞（dendritic cells，DC）影响肿瘤抗原特异性的T细胞免疫应答新机制，相比于野生型小鼠，YTHDF1敲除小鼠表现出较强的肿瘤抗原特异性CD8+T细胞的应答，YTHDF1可能成为免疫治疗的治疗靶点[41]。但是，m6A修饰如何与肿瘤微环境、肿瘤细胞的逃逸和代谢相联系，如何发挥抗肿瘤作用，还需要科研学者进一步的研究。
在癌症的发展过程中，肿瘤细胞的免疫逃逸和能量代谢重新编程紧密交织在一起。肿瘤细胞在争夺葡萄糖方面胜过T细胞，导致抗PD-1治疗的反应受限[42]，因此，靶向肿瘤糖酵解可能是克服抗PD-1 治疗在HCC中的耐药性的一种新型策略[43]。circRHBDD1非编码RNA均起到了增强肿瘤细胞有氧糖酵解作用，增加了抗PD-1药物耐药性。circRHBDD1与YTHDF1相互作用，并在m6A中增强PIK3R1的翻译，通过PI3K/AKT信号通路增加肿瘤细胞有氧糖酵解，降低HCC患者CD8+的比例，造成免疫逃逸。此外，circRHBDD1抑制可以与抗PD-1治疗协同作用，靶向circRHBDD1/YTHDF1/PIK3R1轴可能为HCC新的治疗方式[28]。
BTBD10的表达与肿瘤浸润的B细胞、T细胞、巨噬细胞、中性粒细胞和树突状细胞呈正相关；并且BTBD10与m6A甲基化修饰呈正相关，包括METTL3、METTL14、WTAP、FTO、ALKBH5、YTHDC1、YThDF1-3、IGF2BP1-3，这种相关性为提高靶向药物的有效率提供了新的视角[44]。
结语
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RNA m6A修饰在肿瘤研究中日益受到关注，大量的研究揭示了其在癌症发生发展过程的作用，为癌症的早期诊断和靶向药物的开发提供了新的思路与方法，但其在HCC中与靶蛋白之间的相互作用却十分复杂，功能也各有不同。本文根据HCC发生、发展、预后差、易复发等特点，对m6A甲基化修饰在HCC的侵袭与转移、调控肿瘤微环境的免疫治疗方面进行总结，规律性探索有关HCC的m6A修饰与非编码RNA的互相作用以及在免疫治疗方面的新发现。但是，m6A甲基化修饰靶向性明确的药物还并未进一步开发，与非编码RNA相互作用的靶向性治疗建模还未明确，根据肿瘤细胞的免疫逃逸和代谢进行的免疫靶向治疗方案还未成体系，这些问题是HCC未来诊断与创新药物发现中需进一步探讨的问题。
基金
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  • 河南省科技攻关项目(242102310547)
  • 河南省高等学校青年骨干教师培养计划(2020GGJS108)
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2025年第44卷第4期
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doi: 10.14109/j.cnki.xyylc.2025.04.03
  • 接收时间：2023-07-24
  • 首发时间：2025-12-15
  • 出版时间：2025-04-25
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  • 收稿日期：2023-07-24
  • 录用日期：2024-12-02
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河南省科技攻关项目(242102310547)
河南省高等学校青年骨干教师培养计划(2020GGJS108)
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    河南中医药大学，河南　郑州　450046
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2种不同金属材料的力学参数
科
Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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