ObjectiveTo investigate the difference of DNA methylation before and after bariatric surgery.MethodThe relevant literatures of the research on the changes of DNA methylation level and gene expression regulation in blood and tissues before and after bariatric surgery were retrieved and reviewed.ResultsDNA methylation was an important method of epigenetic regulation in organisms and its role in bariatric surgery had been paid more and more attention in recent years. Existing studies had found that there were changes of DNA methylation in blood and tissues before and after bariatric surgery. The degree of methylation varies with different follow-up time after bariatric surgery and the same gene had different degrees of methylation in different tissues, and some even had the opposite results.ConclusionsDNA methylation levels before and after bariatric surgery are different in different tissues. And studies with larger sample size and longer follow-up time are needed, to further reveal relationship among DNA methylation, obesity, and bariatric surgery.
Objective To review the advance of gene diagnosis and gene therapy on gastric cancer. Methods Literatures about the advance of gene diagnosis and therapy on gastric cancer were reviewed. Results Detection of tumor marker by gene technique is important for early diagnosis, follow-up and therapy evaluation of gastric cancer in clinic. But there are still many problems in gene therapy of gastric cancer. Conclusion Gene detection and gene therapy will become important supplementary means for diagnosis and treatment of gastric cancer.
ObjectiveTo systematically review the effectiveness and safety of demethylation agents in patients with myelodysplastic syndrome.
MethodsRandomized controlled trials (RCTs) about demethylation agents in treating myelodysplastic syndrome was electronically searched in PubMed, EMbase, The Cochrane Library (Issue 3, 2013), Web of Science, CNKI, VIP, WanFang Data and CBM from inception to March 2013. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted data, and assessed methodological quality of the included studies. Meta-analysis was performed using RevMan 5.1 software.
ResultsA total of 4 studies involving 816 patients were finally included. The results of meta-analysis showed that:for patients with myelodysplastic syndrome at middle/advanced stage, compared with the best supportive treatment plan, demethylation agents improved complete remission (CR) (OR=19.14, 95%CI 5.33 to 68.7, P < 0.000 01), partial remission (PR) (OR=20.63, 95%CI 5.76 to 73.93, P < 0.000 01), hematological improvement (HI) (OR=3.58, 95%CI 2.40 to 5.34, P < 0.000 01), and the incidences of Grade Ⅲ or Ⅳ neutropenia (OR=3.82, 95%CI 2.67 to 5.47, P < 0.000 01), Grade Ⅲ or Ⅳ thrombocytopenia (OR=3.98, 95%CI 2.55 to 6.23, P < 0.000 01), and mortalities (OR=0.52, 95%CI 0.35 to 0.77, P < 0.000 01), all with significant differences; and part of patients suffered from Grade Ⅲ or Ⅳ thrombocytopenia and tolerable adverse reaction caused by non-hematologic change.
ConclusionCurrent evidence suggests that demethylation agents in treating myelodysplastic syndrome have apparently curative effects. Besides, it could prolong the time of turning into acute myelocytic leukemia, reduce mortalities, and improve patients' quality of life.
Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes, characterized by high blindness rates and a severe impact on patients' quality of life. Despite adequate glycemic control, some patients exhibit persistent progression of retinal microvascular damage, known as the "metabolic memory" phenomenon. Studies have revealed that the essence of this phenomenon is the sustained expression of epigenetic reprogramming induced by metabolic stress, in which abnormal mitochondrial DNA (mtDNA) methylation plays a pivotal role. Metabolic abnormalities such as hyperglycemia, hyperhomocysteinemia, and hyperlipidemia can alter mtDNA methylation patterns, triggering cascading pathological processes including oxidative stress, chronic inflammation, and neurovascular network disorders, remodeling mitochondrial energy metabolism, and promoting the evolution of DR from subclinical compensatory stage to irreversible structural damage. Abnormal mtDNA methylation serves as a hallmark of metabolic memory and a core driver of microvascular lesions, providing an important theoretical basis for in-depth analysis of metabolic memory mechanisms and exploration of DR intervention strategies. Current research needs to further elucidate its role in DR. Future efforts require integration of multi-dimensional epigenetic biomarkers, precise intervention approaches, and clinical translational research to advance the early diagnosis and individualized treatment of DR.
ObjectiveTo summarize the current research status of the relationship between DNA methylation and liver regeneration.MethodThe related literatures at home and abroad were searched to review the studies on relationships between the methylation level of liver cells, regulation of gene expression, and methylation related proteins and liver regeneration.ResultsThe DNA methylation was an important epigenetic regulation method in vivo and its role in the liver regeneration had been paid more and more attentions in recent years. The existing studies had found the epigenetic phenomena during the liver regeneration such as the genomic hypomethylation, methylation changes of related proliferating genes and DNA methyltransferase and UHRF1 regulation of the liver regeneration.ConclusionsThere are many relationships between DNA methylation and liver regeneration. Regulation of liver regeneration from DNA methylation level is expected to become a reality in the near future.
Retinoblastoma (RB) is a common intraocular tumor in children, often leading to blindness or disability, and its pathogenesis involves genetic and epigenetic regulation. Epigenetics regulates gene expression through mechanisms such as DNA methylation and histone modification without altering the DNA sequence, and the imbalance of its homeostasis is considered a crucial factor in the development and progression of RB. Therapeutic strategies targeting these abnormal modifications offer new potential treatment avenues for RB. Although current research has highlighted the importance of epigenetics in RB, the specific mechanisms of action, the relationship with genetic bases, and the development of targeted drugs remain largely unknown. Therefore, further in-depth research into the epigenetic mechanisms of RB is of great significance for elucidating its carcinogenic mechanisms, identifying effective therapeutic targets, and developing new drugs.
ObjectiveTo determine the level of CDH1 gene promoter hypermethylation in human gastric carcinoma by establishing MS-PCR method, and analyze retrospectively the possible statistical relationship between CDH1 gene promoter hypermethylation in human gastric carcinoma and HP infection, tumor differentiation, invasion, lymph nodal and distant metastasis, respectively.
MethodsThe bisulfite conversion MS-PCR method was adopted to examine the level of CDH1 gene promoter hypermethylation in 40 cases of human gastric carcinoma tissue collected between January 2008 and December 2009. The statistical relationship between CDH1 gene promoter hypermethylation in human gastric carcinoma and HP infection, tumor differentiation, invasion, lymph nodal and distant metastasis were examined respectively with SPSS statistical tools.
ResultsThe positive rate of CDH1 gene promoter hypermethylation in gastric carcinomas (67.5%) was higher than that in paired normal gastric mucosae (12.5%), and the difference was significant (P<0.05). In gastric carcinomas, the positive rate of CDH1 gene promoter hypermethylation in well differentiated or moderately differentiated groups (22.2%) was lower than that in poorly differentiated groups (80.6%), and the difference was significant (P<0.05). The positive rate of CDH1 gene promoter hypermethylation in HP positive groups (78.1%) was higher than that in HP negative groups (25.0%), and the difference was significant (P<0.05).
ConclusionCDH1 gene promoter hypermethylation may play an important role in the process of tumor carcinogenesis in gastric carcinomas. Meanwhile, the CDH1 gene promoter hypermethylation may lead to poor differentiation in gastric carcinomas. CDH1 gene promoter hypermethylation is related to HP infection in the original gastric carcinomas, which shows that HP may get involved in the process of tumor suppressor gene methylation/inactivation and tumor development process.
Pulmonary arterial hypertension (PAH) is a fatal and complex disease characterized by multifactorial involvement in pulmonary vascular remodeling, leading to heart failure. It is difficult to treat and has a poor long-term prognosis. Recent studies highlight the significant role of epigenetic modulation in the pathophysiological progression of PAH, offering new therapeutic approaches to improve clinical outcomes. This article summarizes the role of epigenetic modulation in the development and progression of PAH, focusing on deoxyribonucleic acid methylation, ribonucleic acid methylation, histone modifications, and non-coding ribonucleic acid, in order to understand the role of epigenetic modulation in PAH and identifying new evaluation indexes and therapeutic targets, thereby improving the prognosis of PAH.
Objective To investigate the role of DNA methylation on regulation of cell apoptosis and proliferation in ischemia-reperfusion of small intestine. Methods Thirty-five male Wistar rats were randomly divided into normal group， sham operation group， and ischemia-reperfusion group. The apoptotic cell was assessed by TUNEL and electron microscopy and the expression of Ki-67 was examined by immunohistochemistry in the small intestinal parts （villi epithe-lium， crypt epithelium， and lamina propria mucosa of small intestine）. The DNA methylation was detected by DNA histo-endonuclease-linked detection of methylated DNA sites. Results ①The apoptotic positive cells increased at 3 h， 6 h，and 12 h after ischemia-reperfusion in the villi epithelium， crypt epithelium， and lamina propria mucosa of small intestine as compared with the normal group and sham operation group （P＜0.01）；Moreover， the apoptotic cells in the lamina propria mucosa of small intestine were identified as T cells by electron microscopy. ②The expressions of Ki-67 markedly increased at 3 h， 6 h， 12 h， and 24 h after ischemia-reperfusion in the villi epithelium cells as compared with the normal group and sham operation group （P＜0.01）. ③The weak expression of DNA methylation was found in the villi epith-elium and crypt epithelium in the normal group and sham operation group， the b expression was examined in the crypt epithelium cells nearby stem cell site in the ischemia-reperfusion of small intestine， the change of expression was gradually weak from crypt epithelium to villi epithelium. Conclusion This initial results indicate that the DNA methyl-ation in the ischemia-reperfusion of small intestine might regulate cell apoptosis and proliferation.
Lung cancer is the most common malignant tumor in the world and the leading cause of cancer-related death. Due to the lack of effective early diagnosis methods, the prognosis of lung cancer is poor, but compared with advanced lung cancer, the survival rate of early lung cancer is greatly improved. Therefore, early diagnosis of lung cancer is crucial. As a major epigenetic modification, DNA methylation plays an important role in the development of lung cancer. A large number of studies have shown that detection of tumor suppressor gene methylation is an ideal early diagnosis method for lung cancer. With the continuous improvement of detection technology, methylation detection of multiple genes can be achieved. And it is found that multi-gene methylation combined detection of tissue samples obtained by minimally invasive operation such as puncture of diseased tissue and puncture of lymph node tissue, as well as the noninvasive samples such as peripheral blood, bronchoalveolar lavage fluid and sputum have higher detection rate and higher sensitivity and specificity than single gene methylation. It is an ideal method for early diagnosis of lung cancer.
