随着经济和社会的发展,代谢性疾病的患病率逐年升高,已为全球带来巨大的疾病负担。甲基转移酶样蛋白(Methyltransferase-Like Proteins, METTLs)可调控表观遗传学机制,已成为近年来新兴的研究热点。文章就METTL家族调控三大代谢性疾病...随着经济和社会的发展,代谢性疾病的患病率逐年升高,已为全球带来巨大的疾病负担。甲基转移酶样蛋白(Methyltransferase-Like Proteins, METTLs)可调控表观遗传学机制,已成为近年来新兴的研究热点。文章就METTL家族调控三大代谢性疾病的分子机制作一综述,涉及调控胰岛β细胞功能、胰岛素抵抗、脂肪生成、脂质代谢、血糖稳态等多个方面。希望未来可继续进行更为广泛和深层次的研究,为多种代谢性疾病的诊疗提供理论依据。With the advancement of socioeconomic development, the prevalence of metabolic diseases has been steadily increasing, imposing a significant disease burden globally. Methyltransferase-Like Proteins (METTLs), which regulate epigenetic mechanisms, have emerged as a burgeoning research focus in recent years. This review comprehensively summarizes the molecular mechanisms by which METTL family members regulate three major metabolic diseases, including their roles in modulating pancreatic β-cell function, insulin resistance, adipogenesis, lipid metabolism, and glucose homeostasis. We anticipate that further extensive and in-depth investigations will provide a theoretical foundation for the diagnosis and treatment of diverse metabolic disorders.展开更多
Objective:To investigate the biological functions and molecular regulatory mechanisms of kinesin family member 11(KIF11)in colorectal cancer(CRC).Methods:The expression of KIF11 in CRC was examined by qRT⁃PCR and publ...Objective:To investigate the biological functions and molecular regulatory mechanisms of kinesin family member 11(KIF11)in colorectal cancer(CRC).Methods:The expression of KIF11 in CRC was examined by qRT⁃PCR and public databases.Functional assays(CCK⁃8,colony formation,EdU,and Transwell)were employed to evaluate KIF11’s roles in CRC progression.Western blot,RIP⁃qPCR,MeRIP⁃qPCR,and RNA stability assays were performed to elucidate the molecular mechanism of N6⁃methyladenosine(m6A)modification for KIF11.RNA sequencing(RNA⁃seq)and correlation analysis were used to examine the downstream mechanism of KIF11 regulation.Results:KIF11 was highly expressed in CRC and promoted CRC proliferation and migration.Mechanistically,methyltransferase⁃like 3(METTL3)/insulin like growth factor 2 mRNA binding protein 2(IGF2BP2)enhanced KIF11 mRNA stability and expression in an m6A⁃dependent way.Furthermore,by means of the PROM1/PI3K/AKT pathway,KIF11 facilitated the progression of CRC.Conclusion:The m6A modification of KIF11 by METTL3/IGF2BP2 contributes to CRC progression via the PI3K/AKT signaling pathway,highlighting its potential as a prognostic biomarker and therapeutic target.展开更多
Background:Lung cancer remains the primary cause of mortality worldwide.Methylation modifications of eukaryotic messenger RNA(mRNA),recognized as one of the most prevalent chemical alterations,significantly impact the...Background:Lung cancer remains the primary cause of mortality worldwide.Methylation modifications of eukaryotic messenger RNA(mRNA),recognized as one of the most prevalent chemical alterations,significantly impact the stability,splicing,and translation of mRNA.Methyltransferase-like 21A(METTL21A)functions as a non-histone methyltransferase.The role of methylation-related compounds in the development of cancer has garnered increasing interest in recent years.Methods:The expression levels of METTL21A were assessed in 86 lung cancer samples and 78 adjacent non-cancerous tissues from Taizhou Hospital.Gene expression data were sourced from The Cancer Genome Atlas(TCGA)and Gene Expression Omnibus(GEO)databases.Multi-omics studies were conducted to examine the biological role of METTL21A within lung cancer.We thoroughly explored the potential functions and prognostic implications of METTL21A in this context.Results:An elevated expression of METTL21A was observed in lung cancer tissues.Furthermore,high levels of METTL21A expression correlate with various factors,including age,sex,race,tumor protein P53(TP53)mutations,cancer type,metastasis,and the pathological stage of lung cancer patients,indicating a relationship with poor prognosis.Additionally,METTL21A may affect lung cancer patient outcomes through distinct patterns of immune cell infiltration.Conclusion:METTL21A emerges as a promising candidate prognostic biomarker linked to immune invasion in lung cancer.展开更多
N6-methyladenosine(m6A)modification,one of the most prevalent RNA epi-genetic modifications in eukaryotes,constitutes over 60%of all RNA methylation modifications.This dynamic modification regulates RNA processing,mat...N6-methyladenosine(m6A)modification,one of the most prevalent RNA epi-genetic modifications in eukaryotes,constitutes over 60%of all RNA methylation modifications.This dynamic modification regulates RNA processing,maturation,nucleocytoplasmic transport,translation efficiency,phase separation,and sta-bility,thereby linking its dysregulation to diverse physiological and pathological processes.METTL3,a core catalytic component of the methyltransferase complex responsible for m6A deposition,is frequently dysregulated in diseases,including colorectal cancer(CRC).Although METTL3’s involvement in CRC pathogenesis has been documented,its precise molecular mechanisms and functional roles remain incompletely understood.METTL3 mediates CRC progression-encompa-ssing proliferation,invasion,drug resistance,and metabolic reprogramming-through m6A-dependent modulation of both coding RNAs and noncoding RNAs.Its regulatory effects are primarily attributed to interactions with key signaling pathways at multiple stages of CRC development.Emerging evidence highlights METTL3 as a promising biomarker for CRC diagnosis and prognosis,as well as a potential therapeutic target.By synthesizing recent advances in METTL3 research within CRC,this review provides critical insights into novel strategies for clinical diagnosis and targeted therapy.展开更多
Correction to“METTL5 promotes cell proliferation,invasion,and migration by up-regulating Toll-like receptor 8 expression in colorectal cancer”in World J Gastrointest Oncol 2024;16(5):2006-2017,published by Kong LS,T...Correction to“METTL5 promotes cell proliferation,invasion,and migration by up-regulating Toll-like receptor 8 expression in colorectal cancer”in World J Gastrointest Oncol 2024;16(5):2006-2017,published by Kong LS,Tao R,Li YF,Wang WB,and Zhao X.In this article,we added the correct images.展开更多
文摘随着经济和社会的发展,代谢性疾病的患病率逐年升高,已为全球带来巨大的疾病负担。甲基转移酶样蛋白(Methyltransferase-Like Proteins, METTLs)可调控表观遗传学机制,已成为近年来新兴的研究热点。文章就METTL家族调控三大代谢性疾病的分子机制作一综述,涉及调控胰岛β细胞功能、胰岛素抵抗、脂肪生成、脂质代谢、血糖稳态等多个方面。希望未来可继续进行更为广泛和深层次的研究,为多种代谢性疾病的诊疗提供理论依据。With the advancement of socioeconomic development, the prevalence of metabolic diseases has been steadily increasing, imposing a significant disease burden globally. Methyltransferase-Like Proteins (METTLs), which regulate epigenetic mechanisms, have emerged as a burgeoning research focus in recent years. This review comprehensively summarizes the molecular mechanisms by which METTL family members regulate three major metabolic diseases, including their roles in modulating pancreatic β-cell function, insulin resistance, adipogenesis, lipid metabolism, and glucose homeostasis. We anticipate that further extensive and in-depth investigations will provide a theoretical foundation for the diagnosis and treatment of diverse metabolic disorders.
基金江苏省卫生健康委员会医学科研重点项目(K2023024)789 Outstanding Talent Program of SAHNMU(789ZYRC202090147)。
文摘Objective:To investigate the biological functions and molecular regulatory mechanisms of kinesin family member 11(KIF11)in colorectal cancer(CRC).Methods:The expression of KIF11 in CRC was examined by qRT⁃PCR and public databases.Functional assays(CCK⁃8,colony formation,EdU,and Transwell)were employed to evaluate KIF11’s roles in CRC progression.Western blot,RIP⁃qPCR,MeRIP⁃qPCR,and RNA stability assays were performed to elucidate the molecular mechanism of N6⁃methyladenosine(m6A)modification for KIF11.RNA sequencing(RNA⁃seq)and correlation analysis were used to examine the downstream mechanism of KIF11 regulation.Results:KIF11 was highly expressed in CRC and promoted CRC proliferation and migration.Mechanistically,methyltransferase⁃like 3(METTL3)/insulin like growth factor 2 mRNA binding protein 2(IGF2BP2)enhanced KIF11 mRNA stability and expression in an m6A⁃dependent way.Furthermore,by means of the PROM1/PI3K/AKT pathway,KIF11 facilitated the progression of CRC.Conclusion:The m6A modification of KIF11 by METTL3/IGF2BP2 contributes to CRC progression via the PI3K/AKT signaling pathway,highlighting its potential as a prognostic biomarker and therapeutic target.
基金supported by the Shenzhen Municipal Government of China(No.JCYJ20180507184647104)the Natural Science Foundation of Guangdong Province(Nos.2021A1515011426,2023A1515012585)。
文摘Background:Lung cancer remains the primary cause of mortality worldwide.Methylation modifications of eukaryotic messenger RNA(mRNA),recognized as one of the most prevalent chemical alterations,significantly impact the stability,splicing,and translation of mRNA.Methyltransferase-like 21A(METTL21A)functions as a non-histone methyltransferase.The role of methylation-related compounds in the development of cancer has garnered increasing interest in recent years.Methods:The expression levels of METTL21A were assessed in 86 lung cancer samples and 78 adjacent non-cancerous tissues from Taizhou Hospital.Gene expression data were sourced from The Cancer Genome Atlas(TCGA)and Gene Expression Omnibus(GEO)databases.Multi-omics studies were conducted to examine the biological role of METTL21A within lung cancer.We thoroughly explored the potential functions and prognostic implications of METTL21A in this context.Results:An elevated expression of METTL21A was observed in lung cancer tissues.Furthermore,high levels of METTL21A expression correlate with various factors,including age,sex,race,tumor protein P53(TP53)mutations,cancer type,metastasis,and the pathological stage of lung cancer patients,indicating a relationship with poor prognosis.Additionally,METTL21A may affect lung cancer patient outcomes through distinct patterns of immune cell infiltration.Conclusion:METTL21A emerges as a promising candidate prognostic biomarker linked to immune invasion in lung cancer.
基金Supported by Jiangxi Provincial Natural Science Foundation,No.20242BAB25454the Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular of Ministry of Education of Gannan Medical University,No.XN202013+1 种基金Science and Technology Research Project of Jiangxi Provincial Department of Education,No.GJJ201528Startup Foundation for Advanced Talents of Gannan Medical University,No.QD202124.
文摘N6-methyladenosine(m6A)modification,one of the most prevalent RNA epi-genetic modifications in eukaryotes,constitutes over 60%of all RNA methylation modifications.This dynamic modification regulates RNA processing,maturation,nucleocytoplasmic transport,translation efficiency,phase separation,and sta-bility,thereby linking its dysregulation to diverse physiological and pathological processes.METTL3,a core catalytic component of the methyltransferase complex responsible for m6A deposition,is frequently dysregulated in diseases,including colorectal cancer(CRC).Although METTL3’s involvement in CRC pathogenesis has been documented,its precise molecular mechanisms and functional roles remain incompletely understood.METTL3 mediates CRC progression-encompa-ssing proliferation,invasion,drug resistance,and metabolic reprogramming-through m6A-dependent modulation of both coding RNAs and noncoding RNAs.Its regulatory effects are primarily attributed to interactions with key signaling pathways at multiple stages of CRC development.Emerging evidence highlights METTL3 as a promising biomarker for CRC diagnosis and prognosis,as well as a potential therapeutic target.By synthesizing recent advances in METTL3 research within CRC,this review provides critical insights into novel strategies for clinical diagnosis and targeted therapy.
文摘Correction to“METTL5 promotes cell proliferation,invasion,and migration by up-regulating Toll-like receptor 8 expression in colorectal cancer”in World J Gastrointest Oncol 2024;16(5):2006-2017,published by Kong LS,Tao R,Li YF,Wang WB,and Zhao X.In this article,we added the correct images.
