Background: Suppressor 3 of cytokine signaling (SOCS3) hypermethylation has been reported to participate in hepatocellular carcinoma (HCC) development and progression, but conflicting results were published. This study aimed to analyze the clinical effects of SOCS3 hypermethylation in HCC and the effects of sex and age on SOCS3 hypermethylation in HCC.
Methods: Databases were searched for relevant case-control and cohort studies on SOCS3 hypermethylation in HBV-related HCC. In vitro and in vivo studies and studies of patients with serious comorbidities were excluded. Review Manager 5.2 was used to estimate the effects of the results among the selected studies. Forest plots, sensitivity analysis, and bias analysis for the included studies were also conducted.
Results: Finally, 8 relevant studies met the inclusion criteria. A significant difference in SOCS3 hypermethylation in HCC was found between tumor and nontumor groups (the odds ratio [OR] = 2.01, 95% confidence interval [CI]: 1.48-2.73, P < .00001; P for heterogeneity = .39, I2 = 5%). The meta-analysis suggested no significant difference in the effect of sex (OR = 1.00, 95% CI: 0.76-1.31, P = .76; P for heterogeneity = .44, I2 = 0%) and age on SOCS3 hypermethylation in HCC (OR = 1.11, 100% CI: 0.78-1.29, P = .03; P for heterogeneity = .14, I2 = 36%). Limited publication bias was observed in this study.
Conclusion: SOCS3 hypermethylation is associated with HBV-related HCC. Sex and age do not affect the association between SOCS3 hypermethylation and HCC. SOCS3 might be a treatment target for HCC.
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http://dx.doi.org/10.1097/MD.0000000000027604 | DOI Listing |
Clin Epigenetics
May 2024
Division of Nutrition, St. John's Research Institute, St. John's Medical College, St Johns National Academy of Health Sciences, Sarjapura Road, Koramangala, Bangalore, 560034, India.
Objective: DNA methylation influences gene expression and function in the pathophysiology of type 2 diabetes mellitus (T2DM). Mapping of T2DM-associated DNA methylation could aid early detection and/or therapeutic treatment options for diabetics.
Design: A systematic literature search for associations between T2DM and DNA methylation was performed.
Cell Death Differ
May 2023
MOE Joint International Research Laboratory of Animal Health and Food Safety, Nanjing Agricultural University, Nanjing, Jiangsu, PR China.
Hepatic stellate cells (HSC) are key effector cells in liver fibrosis. Upon stimulation, the quiescent HSC undergoes complex morphological and functional changes to transdifferentiate into activated collagen-producing myofibroblasts. DNA/RNA methylations (5mC/mA) are both implicated to participate in hepatic fibrosis, yet their respective roles and specific targets in HSC activation remain elusive.
View Article and Find Full Text PDFBr J Haematol
May 2023
Department of Biology, Universidad Autónoma de Madrid, Madrid, Spain.
Int J Mol Sci
June 2022
Inserm U1283, CNRS UMR 8199, European Genomic Institute for Diabetes, Institut Pasteur de Lille, 59000 Lille, France.
Excessive fetal growth is associated with DNA methylation alterations in human hematopoietic stem and progenitor cells (HSPC), but their functional impact remains elusive. We implemented an integrative analysis combining single-cell epigenomics, single-cell transcriptomics, and in vitro analyses to functionally link DNA methylation changes to putative alterations of HSPC functions. We showed in hematopoietic stem cells (HSC) from large for gestational age neonates that both DNA hypermethylation and chromatin rearrangements target a specific network of transcription factors known to sustain stem cell quiescence.
View Article and Find Full Text PDFHum Cell
July 2022
Departments of Biochemistry, Medicine, College of Medicine and Health Sciences, Sultan Qaboos University, PC 123, P. O. Box 35, Muscat, Sultanate of Oman.
Gastric cancer (GC) is ranked the third leading cause of cancer-related deaths worldwide. Mutations and epigenetic alterations in several essential genes, including p53, KRAS, PIK3CA, FAT4 and ARID1A, are often reported. Furthermore, loss of SOCS3 expression was reported in GC, suggesting its tumor suppressor role.
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