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| 1 | Role of the Wnt/β-catenin pathway in gastric cancer: An indepth literature review显示文摘Gastric cancer remains one of the most common cancers worldwide and one of the leading cause for cancerrelated deaths. Gastric adenocarcinoma is a multifactorial disease that is genetically, cytologically and architecturally more heterogeneous than other gastrointestinal carcinomas.The aberrant activation of the Wnt/β-catenin signaling pathway is involved in the development and progression of a significant proportion of gastric cancer cases. This review focuses on the participation of the Wnt/b-catenin pathway in gastric cancer by offering an analysis of the relevant literature published in this field. Indeed, it is discussed the role of key factors in Wnt/β-catenin signaling and their downstream effectors regulating processes involved in tumor initiation, tumor growth, metastasis and resistance to therapy. Available data indicate that constitutive Wnt signalling resulting from Helicobacter pylori infection and inactivation of Wnt inhibitors(mainly by inactivating mutations and promoter hypermethylation) play an important role in gastric cancer. Moreover, a number of recent studies confirmed CTNNB1 and APC as driver genes in gastric cancer. The identification of specific membrane, intracellular, and extracellular components of the Wnt pathway has revealed potential targets for gastric cancer therapy. High-throughput 'omics' approaches will help in the search for Wnt pathway antagonist in the near future. | Miguel Angel Chiurillo | 2015 | World Journal of Experimental Medicine2015，5，2： | 58 |
| 2 | Epigenetic regulation: methylation of histone and non-histone proteins显示文摘Histone methylation is believed to play important roles in epigenetic memory in various biological processes. However, questions like whether the methylation marks themselves are faithfully transmit- ted into daughter cells and through what mechanisms are currently under active investigation. Previ- ously, methylation was considered to be irreversible, but the recent discovery of histone lysine de- methylases revealed a dynamic nature of histone methylation regulation on four of the main sites of methylation on histone H3 and H4 tails (H3K4, H3K9, H3K27 and H3K36). Even so, it is still unclear whether demethylases specific for the remaining two sites, H3K79 and H4K20, exist. Furthermore, be- sides histone proteins, the lysine methylation and demethylation also occur on non-histone proteins, which are probably subjected to similar regulation as histones. This review discusses recent pro- gresses in protein lysine methylation regulation focusing on the above topics, while referring readers to a number of recent reviews for the biochemistry and biology of these enzymes. | LAN Fei1 & SHI Yang 2 1 Department of Biology, Constellation Pharmaceuticals, 148 Sidney Street, Cambridge, MA 02139, USA 2 Department of Pathology, Harvard Medical School, 77 Ave Louise Pasteur, Boston MA, 02115, USA | 2009 | Science China(Life Sciences)2009，52，4： | 27 |
| 3 | Diet and microbiota in inflammatory bowel disease: The gut in disharmony显示文摘Bacterial colonization of the gut shapes both the local and the systemic immune response and is implicated in the modulation of immunity in both healthy and disease states. Recently, quantitative and qualitative changes in the composition of the gut microbiota have been detected in Crohn's disease and ulcerative colitis, reinforcing the hypothesis of dysbiosis as a relevant mechanism underlying inflammatory bowel disease(IBD) pathogenesis. Humans and microbes have coexisted and co-evolved for a long time in a mutually beneficial symbiotic association essential for maintaining homeostasis. However, the microbiome is dynamic, changing with age and in response to environmental modifications. Among such environmental factors, food and alimentary habits, progressively altered in modern societies, appear to be critical modulators of the microbiota, contributing to or co-participating in dysbiosis. In addition, food constituents such as micronutrients are important regulators of mucosal immunity, with direct or indirect effects on the gut microbiota. Moreover, food constituents have recently been shown to modulate epigenetic mechanisms, which can result in increased risk for the development and progression of IBD. Therefore, it is likely that a better understanding of the role of different food components in intestinal homeostasis and the resident microbiota will be essential for unravelling the complex molecular basis of the epigenetic, genetic and environment interactions underlying IBD pathogenesis as well as for offering dietary interventions with minimal side effects. | Davy CM Rapozo Claudio Bernardazzi Heitor Siffert Pereira de Souza | 2017 | World Journal of Gastroenterology2017，23，12： | 24 |
| 4 | Reversibility and heritability of liver fibrosis:Implications for research and therapy显示文摘Liver fibrosis continues to be a major health problem worldwide due to lack of effective therapy.If the etiology cannot be eliminated,liver fibrosis progresses to cirrhosis and eventually to liver failure or malignancy;both are associated with a fatal outcome.Liver transplantation,the only curative therapy,is still mostly unavailable.Liver fibrosis was shown to be a reversible process;however,complete reversibility remains debatable.Recently,the molecular markers of liver fibrosis were shown to be transmitted across generations.Epigenetic mechanisms including DNA methylation,histone posttranslational modifications and noncoding RNA have emerged as major determinants of gene expression during liver fibrogenesis and carcinogenesis.Furthermore,epigenetic mechanisms have been shown to be transmitted through mitosis and meiosis to daughter cells and subsequent generations.However,the exact epigenetic regulation of complete liver fibrosis resolution and inheritance has not been fully elucidated.This communication will highlight the recent advances in the search for delineating the mechanisms governing resolution of liver fibrosis and the potential for multigenerational and transgenerational transmission of fibrosis markers.The fact that epigenetic changes,unlike genetic mutations,are reversible and can be modulated pharmacologically underscores the unique opportunity to develop effective therapy to completely reverse liver fibrosis,to prevent the development of malignancy and to regulate heritability of fibrosis phenotype. | Hussein M Atta | 2015 | World Journal of Gastroenterology2015，21，17： | 23 |
| 5 | Update on the management of pancreatic cancer:Surgery is not enough显示文摘Pancreatic ductal adenocarcinoma(PDAC) represents the fourth cause of death in cancer and has a 5-year survival of < 5%.Only about 15% of the patients present with a resectable PDAC with potential to undergo 'curative' surgery.After surgery,local and systemic recurrence,is though very common.The median survival of resected patients with adjuvant chemotherapy after surgery is only 20-23 mo.This underscores the significant need to improve PDAC management strategies.Increased survival rate is dependent on new breakthroughs in our understanding of not at least tumor biology.The aim of this review is to update and comment on recent knowledge concerning PDAC biology and new diagnostics and treatment modalities.One fundamental approach to improve survival rates is by earlier and improved diagnosis of the disease.In recent years,novel blood-based biomarkers have emerged based on genetic,epigenetic and protein changes in PDAC with very promising results.For biomarkers to enter clinical practice they need to have been developed using adequate control groups and provide high sensitivity and specificity and by this identify patients at risk already in a pre-symptomatic stage.Another way to improve outcomes,is by employing neoadjuvant treatments thereby increasing the number of resectable cases.Novel systemic treatment regimes like FOLFIRINOX and nab-paclitaxel have demonstrated improvements in prolonging survival in advanced cases,but long-term survival is still scarce.The future improved understanding of PDAC biology will inevitably render new treatment options directed against both the cancer cells and the surrounding microenvironment. | Daniel Ansari Adam Gustafsson Roland Andersson | 2015 | World Journal of Gastroenterology2015，21，11： | 18 |
| 6 | Biomarkers in colorectal cancer: Current clinical utility and future perspectives显示文摘Colorectal cancer(CRC) is a major cause of cancer death worldwide. CRC has poor prognosis and there is a crucial need for new diagnostic and prognostic biomarkers to avoid CRC-related deaths. CRC can be considered a sporadic disease in most cases(75%-80%), but it has been suggested that crosstalk between gene mutations(i.e., mutations of BRAF, KRAS, and p53 as well as microsatellite instability) and epigenetic alterations(i.e., DNA methylation of Cp G island promoter regions) could play a pivotal role in cancer development. A number of studies have focused on molecular testing to guide targeted and conventional treatments for patients with CRC, sometimes with contrasting results. Some of the most useful innovations in the management of CRC include the possibility to detect the absence of KRAS, BRAF, NRAS and PIK3 CA gene mutations with the subsequent choice to administer targeted adjuvant therapy with anti-epidermal growth factor receptor antibodies. Moreover, CRC patients can benefit from tests for microsatellite instability and for the detection of loss of heterozygosity of chromosome 18 q that can be helpful in guiding therapeutic decisions as regards the administration of 5-FU. The aim of this review was to summarize the most recent evidence on the possible use of genetic or epigenetic biomarkers for diagnosis, prognosis and response to therapy in CRC patients. | Marco Vacante Antonio Maria Borzì Francesco Basile Antonio Biondi | 2018 | World Journal of Clinical Cases2018，6，15： | 18 |
| 7 | Mapping the epigenetic modifications of DNA and RNA显示文摘Over 17 and 160 types of chemical modifications have been identified in DNA and RNA,respectively.The interest in understanding the various biological functions of DNA and RNA modifications has lead to the cutting-edged fields of epigenomics and epitranscriptomics.Developing chemical and biological tools to detect specific modifications in the genome or transcriptome has greatly facilitated their study.Here,we review the recent technological advances in this rapidly evolving field.We focus on high-throughput detection methods and biological findings for these modifications,and discuss questions to be addressed as well.We also summarize third-generation sequencing methods,which enable long-read and single-molecule sequencing of DNA and RNA modification. | Lin-Yong Zhao Jinghui Song Yibin Liu Chun-Xiao Song Chengqi Yi | 2020 | Protein & Cell2020，11，11： | 17 |
| 8 | Influence of environmental factors in the development of inflammatory bowel diseases显示文摘Idiopathic inflammatory bowel diseases(IBD), Crohn's disease(CD) and ulcerative colitis(UC), are multifactorial diseases that are manifested after disruption of a genetic predisposed individual and its intestinal microflora through an environmental stimulus. Urbanization and industrialization are associated with IBD. Epidemiological data, clinical observations and family/immigrants studies indicate the significance of environmental influence in the development of IBD. Some environmental factors have a different effect on the subtypes of IBD. Smoking and appendectomy is negatively associated with UC, but they are aggravating factors for CD. A westernized high fat diet, full of refined carbohydrates is strongly associated with the development of IBD, contrary to a high in fruit, vegetables and polyunsaturated fatty acid-3 diet that is protective against these diseases. High intake of nonsteroidal antiinflammatory drug and oral contraceptive pills as well as the inadequacy of vitamin D leads to an increased risk for IBD and a more malignant course of disease. Moreover, other factors such as air pollution, psychological factors, sleep disturbances and exercise influence the development and the course of IBD. Epigenetic mechanism like DNA methylation, histone modification and altered expression of miR NAS could explain the connection between genes and environmental factors in triggering the development of IBD. | Evangelia Legaki Maria Gazouli | 2016 | World Journal of Gastrointestinal Pharmacology and Therapeutics2016，7，1： | 15 |
| 9 | Retrospective and perspective of plant epigenetics in China显示文摘Epigenetics refers to the study of heritable changes in gene function that do not involve changes in the DNA sequence. Such effects on cellular and physiological phenotypic traits may result from external or environmental factors or be part of normal developmental program. In eukaryotes, DNA wraps on a histone octamer(two copies of H2A, H2B, H3 and H4) to form nucleosome, the fundamental unit of chromatin. The structure of chromatin is subjected to a dynamic regulation through multiple epigenetic mechanisms, including DNA methylation, histone posttranslational modifications(PTMs), chromatin remodeling and noncoding RNAs. As conserved regulatory mechanisms in gene expression, epigenetic mechanisms participate in almost all the important biological processes ranging from basal development to environmental response. Importantly, all of the major epigenetic mechanisms in mammalians also occur in plants. Plant studies have provided numerous important contributions to the epigenetic research. For example, gene imprinting, a mechanism of parental allele-specific gene expression, was firstly observed in maize; evidence of paramutation, an epigenetic phenomenon that one allele acts in a single locus to induce a heritable change in the other allele, was firstly reported in maize and tomato.Moreover, some unique epigenetic mechanisms have been evolved in plants. For example, the 24-nt siRNA-involved RNA-directed DNA methylation(RdDM) pathway is plant-specific because of the involvements of two plant-specific DNA-dependent RNA polymerases, Pol IV and Pol V. A thorough study of epigenetic mechanisms is of great significance to improve crop agronomic traits and environmental adaptability. In this review, we make a brief summary of important progress achieved in plant epigenetics field in China over the past several decades and give a brief outlook on future research prospects.We focus our review on DNA methylation and histone PTMs, the two most important aspects of epigenetic mechanisms. | Cheng-Guo Duan Jian-Kang Zhu Xiaofeng Cao | 2018 | Journal of Genetics and Genomics2018，45，11： | 14 |
| 10 | DNA methylation in human diseases显示文摘Even though the importance of epigenetics was first recognized in light of its role in tissue development,an increasing amount of evidence has shown that it also plays an important role in the development and progression of many common diseases.We discuss some recent findings on one representative epigenetic modification,DNA methylation,in some common diseases.While many new risk factors have been identified through the population-based epigenetic epidemiologic studies on the role of epigenetics in common diseases,this relatively new field still faces many unique challenges.Here,we describe those promises and unique challenges of epigenetic epidemiological studies and propose some potential solutions. | Zelin Jin Yun Liu | 2018 | Genes & Diseases2018，5，1： | 12 |
| 11 | Epigenetic Modifications of mRNA and DNA in Plants显示文摘Advances in the detection and mapping of messenger RNA(mRNA)N^6-methyladenosine(m 6A)and 5-methylcytosine(m 5C),and DNA N^6-methyldeoxyadenosine(6mA)redefined our understanding of these modifications as additional tiers of epigenetic regulation.In plants,the most prevalent internal mRNA modifications,m^6A and m^5C,play crucial and dynamic roles in many processes,including embryo development,stem cell fate determination,trichome branching,leaf morphogenesis,floral transition,stress responses,fruit ripening,and root development.The newly identified and widespread epigenetic marker 6mA DNA methylation is associated with gene expression,plant development,and stress responses.Here,we review the latest research progress on mRNA and DNA epigenetic modifications,including the detection,dynamics,distribution,functions,regulatory proteins,and evolution,with a focus on m^6A,m^5C,and 6mA.We also provide some perspectives on future research of the newly identified and unknown epigenetic modifications of mRNA and DNA in plants. | Zhe Liang Adeel Riaz Sadaruddin Chachar Yike Ding Hai Du Xiaofeng Gu | 2020 | Molecular Plant2020，13，1： | 12 |
| 12 | Drug resistance and combating drug resistance in cancer显示文摘Cancer is the second leading cause of death in the US.Current major treatments for cancer management include surgery,cytotoxic chemotherapy,targeted therapy,radiation therapy,endocrine therapy and immunotherapy.Despite the endeavors and achievements made in treating cancers during the past decades,resistance to classical chemotherapeutic agents and/or novel targeted drugs continues to be a major problem in cancer therapies.Drug resistance,either existing before treatment(intrinsic)or generated after therapy(acquired),is responsible for most relapses of cancer,one of the major causes of death of the disease.Heterogeneity among patients and tumors,and the versatility of cancer to circumvent therapies make drug resistance more challenging to deal with.Better understanding the mechanisms of drug resistance is required to provide guidance to future cancer treatment and achieve better outcomes.In this review,intrinsic and acquired resistance will be discussed.In addition,new discoveries in mechanisms of drug resistance will be reviewed.Particularly,we will highlight roles of ATP in drug resistance by discussing recent findings of exceptionally high levels of intratumoral extracellular ATP as well as intracellular ATP internalized from extracellular environment.The complexity of drug resistance development suggests that combinational and personalized therapies,which should take ATP into consideration,might provide better strategies and improved efficacy for fighting drug resistance in cancer. | Xuan Wang Haiyun Zhang Xiaozhuo Chen | 2019 | Cancer Drug Resistance2019，2，2： | 12 |
| 13 | Epigenetics in hepatocellular carcinoma: An update and future therapy perspectives显示文摘Hepatocellular carcinoma(HCC),the predominant form of adult liver malignancies,is a global health concern.Its dismal prognosis has prompted recent significant advances in the understanding of its etiology and pathogenesis.The deregulation of epigenetic mechanisms,which maintain heritable gene expression changes and chromatin organization,is implicated in the development of multiple cancers,including HCC.This review summarizes the current knowledge of epigenetic mechanisms in the pathogenesis of HCC,with an emphasis on HCC mediated by chronic hepatitis B virus infection.This review also discusses the encouraging outcomes and lessons learnt from epigenetic therapies for hematological and other solid cancers,and highlights the future potential of similar therapies in the treatment of HCC. | Li Ma Mei-Sze Chua Ourania Andrisani Samuel So | 2014 | World Journal of Gastroenterology2014，20，2： | 12 |
| 14 | DNA methylation in gastric cancer, related to Helicobacter pylori and Epstein-Barr virus显示文摘Gastric cancer is a leading cause of cancer death worldwide,and significant effort has been focused on clarifying the pathology of gastric cancer.In particular,the development of genome-wide analysis tools has enabled the detection of genetic and epigenetic alterations in gastric cancer;for example,aberrant DNA methylation in gene promoter regions is thought to play a crucial role in gastric carcinogenesis.The etiological viewpoint is also essential for the study of gastric cancers,and two distinct pathogens,Helicobacter pylori(H.pylori)and Epstein-Barr virus(EBV),are known to participate in gastric carcinogenesis.Chronic inflammation of the gastric epithelium due to H.pylori infection induces aberrant polyclonal methylation that may lead to an increased risk of gastric cancer.In addition,EBV infection is known to cause extensive methylation,and EBV-positive gastric cancers display a high methylation epigenotype,in which aberrant methylation extends to not only Polycomb repressive complex(PRC)-target genes in embryonic stem cells but also non-PRC-target genes.Here,we review aberrant DNA methylation in gastric cancer and the association between methylation and infection with H.pylori and EBV. | Keisuke Matsusaka Sayaka Funata Masashi Fukayama Atsushi Kaneda | 2014 | World Journal of Gastroenterology2014，20，14： | 12 |
| 15 | Functions and mechanisms of plant histone deacetylases显示文摘Lysine acetylation, one of the major types of post-translational modifications, plays critical roles in regulating gene expression and protein function. Histone deacetylases(HDACs) are responsible for removing acetyl groups from lysines of both histone and non-histone proteins. While tremendous progress has been made in understanding the function and mechanism of HDACs in animals in the past two decades, nearly half of the HDAC studies in plants were reported within the past five years. In this review,we summarize the major findings on plant HDACs, with a focus on the model plant Arabidopsis thaliana, and highlight the components, regulatory mechanisms, and biological functions of HDAC complexes. | Xiangsong Chen Adeline BDing Xuehua Zhong | 2020 | Science China(Life Sciences)2020，63，2： | 11 |
| 16 | Deacetylase inhibitors-focus on non-histone targets and effects显示文摘Inhibitors of protein deacetylases have recently been established as a novel therapeutic principle for several human diseases,including cancer.The original notion of the mechanism of action of these compounds focused on the epigenetic control of transcriptional processes, especially of tumor suppressor genes,by interfering with the acetylation status of nuclear histone proteins,hence the name histone deacetylase inhibitors was coined.Yet,this view could not explain the high specificity for tumor cells and recent evidence now suggests that non-histone proteins represent major targets for protein deacetylase inhibitors and that the post-translational modification of the acetylome is involved in various cellular processes of differentiation,survival and cell death induction. | Matthias Ocker | 2010 | World Journal of Biological Chemistry2010，1，5： | 11 |
| 17 | DNA methylation,microRNAs,and their crosstalk as potential biomarkers in hepatocellular carcinoma显示文摘Epigenetic alterations have been identified as a major characteristic in human cancers.Advances in the field of epigenetics have contributed significantly in refining our knowledge of molecular mechanisms underlying malignant transformation.DNA methylation and microRNA expression are epigenetic mechanisms that are widely altered in human cancers including hepatocellular carcinoma(HCC),the third leading cause of cancer related mortality worldwide.Both DNA methylation and microRNA expression patterns are regulated in developmental stage specific-,cell type specific-and tissue-specific manner.The aberrations are inferred in the maintenance of cancer stem cells and in clonal cell evolution during carcinogenesis.The availability of genome-wide technologies for DNA methylation and microRNA profiling has revolutionized the field of epigenetics and led to the discovery of a number of epigenetically silenced microRNAs in cancerous cells and primary tissues.Dysregulation of these microRNAs affects several key signalling pathways in hepatocarcinogenesis suggesting that modulation of DNA methylation and/or microRNA expression can serve as new therapeutic targets for HCC.Accumulative evidence shows that aberrant DNA methylation of certain microRNA genes is an event specifically found in HCC which correlates with unfavorable outcomes.Therefore,it can potentially serve as a biomarker for detection as well as for prognosis,monitoring and predicting therapeutic responses in HCC. | Sumadi Lukman Anwar Ulrich Lehmann | 2014 | World Journal of Gastroenterology2014，20，24： | 11 |
| 18 | JMJD3 in the regulation of human diseases显示文摘In recent years,many studies have shown that histone methylation plays an important role in maintaining the active and silent state of gene expression in human diseases.The Jumonji domain-containing protein D3(JMJD3),specifically demethylate di-and trimethyllysine 27 on histone H3(H3K27me2/3),has been widely studied in immune diseases,infectious diseases,cancer,developmental diseases,and aging related diseases.We will focus on the recent advances of JMJD3 function in human diseases,and looks ahead to the future of JMJD3 gene research in this review. | Xiangxian Zhang Li Liu Xia Yuan Yuquan Wei Xiawei | 2019 | Protein & Cell2019，10，12： | 10 |
| 19 | Metabolic reprogramming and epigenetic modifications on the path to cancer显示文摘Metabolic rewiring and epigenetic remodeling,which are closely linked and reciprocally regulate each other,are among the well-known cancer hallmarks.Recent evi-dence suggests that many metabolites serve as sub-strates or cofactors of chromatin-modifying enzymes as a consequence of the translocation or spatial regional-ization of enzymes or metabolites.Various metabolic alterations and epigenetic modifications also reportedly drive immune escape or impede immunosurveillance within certain contexts,playing important roles in tumor progression.In this review,we focus on how metabolic reprogramming of tumor cells and immune cells reshapes epigenetic alterations,in particular the acety-lation and methylation of histone proteins and DNA.We also discuss other eminent metabolic modifications such as,succinylation,hydroxybutyrylation,and lacty-lation,and update the current advances in metabolism-and epigenetic modification-based therapeutic pro-spects in cancer. | Linchong Sun Huafeng Zhang Ping Gao | 2022 | Protein & Cell2022，13，12： | 10 |
| 20 | EZH2, an epigenetic driver of prostate cancer显示文摘The histone methyltransferase EZH2 has been in the limelight of the fi eld of cancer epigenetics for a decade now since it was fi rst discovered to exhibit an elevated expression in metastatic prostate cancer.It persists to attract much scientifi c attention due to its important role in the process of cancer development and its potential of being an effective therapeutic target.Thus here we review the dysregulation of EZH2 in prostate cancer,its function,upstream regulators,downstream effectors,and current status of EZH2-targeting approaches.This review there-fore provides a comprehensive overview of EZH2 in the context of prostate cancer. | Yeqing Angela Yang Jindan Yu | 2013 | Protein & Cell2013，4，5： | 9 |
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