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   Home  »  Epigenetic Resources  »  Epigenetic Research Papers 1/6/25 - 1/10/25 
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Epigenetic Research Papers 1/6/25 - 1/10/25


Cong P et. al. (December 2024). DNMT3a Deficiency Contributes to Anesthesia/Surgery-Induced Synaptic Dysfunction and Cognitive Impairment in Aged Mice Aging Cell. :e14458.
This study investigates the role of DNMT3a deficiency in anesthesia and surgery-induced cognitive impairment in aged mice. It demonstrates that reduced DNMT3a levels in hippocampal neurons lead to global DNA hypomethylation, increased LRG1 transcription, and TGF-β signaling activation, contributing to synaptic dysfunction and memory deficits. Restoring DNMT3a or silencing LRG1 mitigates these effects, identifying DNMT3a as a potential therapeutic target for perioperative neurocognitive disorder (PND).
Products Used: MethylFlash Global DNA Methylation (5-mC) ELISA Easy Kit (Colorimetric), MethylFlash Global DNA Hydroxymethylation (5-hmC) ELISA Easy Kit (Colorimetric), EpiQuik Chromatin Immunoprecipitation (ChIP) Kit

Gu L et. al. (January 2025). FBP1 controls liver cancer evolution from senescent MASH hepatocytes Nature.
This study examines the role of fructose-1,6-bisphosphatase 1 (FBP1) in the progression of liver cancer from senescent hepatocytes associated with metabolic-dysfunction steatohepatitis (MASH). FBP1, a p53 target, is elevated in senescent hepatocytes but suppressed during hepatocellular carcinoma (HCC) development via promoter hypermethylation and proteasomal degradation. The study highlights how the NRF2-FBP1-AKT-p53 metabolic switch drives DNA damage, senescence reversal, and proliferation, facilitating the transition from MASH to HCC.
Products Used: EpiQuik Methylated DNA Immunoprecipitation Kit

Wang C et. al. (December 2024). Tumor-derived CCL15 regulates RNA m6A methylation in cancer-associated fibroblasts to promote hepatocellular carcinoma growth Cancer Lett. :217420.
This study explores how tumor-derived CCL15 drives hepatocellular carcinoma (HCC) growth by mediating interactions between cancer cells and cancer-associated fibroblasts (CAFs). CCL15 promotes FTO expression in CAFs via the STAT3 pathway, leading to m6A demethylation of CEBPA mRNA, which upregulates CXCL5—a factor that enhances HCC proliferation through CXCR2 activation. The study identifies a CCL15-CXCL5 feedback loop and highlights CCL15 as a potential therapeutic target in HCC progression.
Products Used: EpiQuik Chromatin Immunoprecipitation (ChIP) Kit

Sharma S et. al. (December 2024). Assessing molecular changes underlying isopropylated phenyl phosphate (IPP)-induced larval sensorimotor response deficits in zebrafish Ecotoxicol Environ Saf. 290:117619.
This study investigates the molecular changes underlying isopropylated phenyl phosphate (IPP)-induced sensorimotor deficits in zebrafish larvae. IPP exposure caused morphological abnormalities, sensorimotor hypoactivity, and increased dopamine levels, alongside disruptions in retinoic acid receptor activity, DNA hypermethylation, and differential gene expression in the eyes. These findings reveal that environmentally relevant concentrations of IPP impact neurometabolomic, genetic, and epigenetic pathways, offering insights into its potential toxicity.
Products Used: MethylFlash Global DNA Methylation (5-mC) ELISA Easy Kit (Colorimetric)

Cui LG et. al. (December 2024). Targeting the ALKBH5-NLRP3 positive feedback loop alleviates cardiomyocyte pyroptosis after myocardial infarction Cui LG et. al. (December 2024).
This study explores the role of the ALKBH5-NLRP3 positive feedback loop in cardiomyocyte pyroptosis following myocardial infarction (MI). Elevated ALKBH5, an m6A RNA demethylase, promotes NLRP3 inflammasome activation, exacerbating pyroptosis, while NLRP3 further enhances ALKBH5 expression. Targeting this feedback loop with small-molecule inhibitors alleviates pyroptosis, offering a potential therapeutic strategy for MI-induced cardiac damage.
Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)

Zhang S et. al. (December 2024).  Knockdown of IGF2BP2 overcomes cisplatin-resistance in lung cancer through downregulating Spon2 gene Hereditas. 161(1):55.
This study examines the role of IGF2BP2 in cisplatin (DDP) resistance in lung cancer. Knockdown of IGF2BP2 reduces the expression of the Spon2 gene via m6A modification, enhancing the efficacy of DDP treatment by inhibiting cell viability and promoting apoptosis in resistant lung cancer cells. These findings suggest that targeting IGF2BP2 could provide a novel strategy for overcoming chemotherapy resistance in lung cancer.
Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)

Kang KA et. al. (January 2025).  Epigenetic Regulation of Nuclear Factor Erythroid-2-Related Factor 2 in Colorectal Cancer Cells Resistant to Ionizing Radiation Biomol Ther (Seoul). 33(1):182-192.
This study investigates the epigenetic regulation of NRF2 in γ-radiation-resistant colorectal cancer cells. Increased expression and promoter hypomethylation of NRF2, driven by TET1 and histone modifications, contribute to enhanced antioxidant defense and radiation resistance. Targeting NRF2 or its epigenetic regulators could improve radiotherapy outcomes in colorectal cancer.
Products Used: Methylamp DNA Modification Kit

Zhang G et. al. (December 2024). SUZ12-Increased NRF2 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Apoptosis, Inflammation, and Ferroptosis Cardiovasc Toxicol.
This study explores the protective role of SUZ12-mediated NRF2 expression in alleviating cardiac ischemia/reperfusion injury. Increased NRF2 levels reduced cardiomyocyte apoptosis, inflammation, and ferroptosis in hypoxia/reoxygenation models and improved cardiac function in acute myocardial infarction (AMI) rat models. These findings highlight NRF2 as a potential therapeutic target for AMI.
Products Used: EpiQuik Nuclear Extraction Kit


Epigenetic Resources
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Suggested Reads:

Enhancer Activation and H3K27ac in Cell-State Plasticity
m6A RNA Methylation in Cancer Immunity and Therapeutic Resistance
cfDNA Methylation in Liquid Biopsy Research: Where Global 5-mC, 5-hmC, Enrichment, and RRBS Readouts Fit
Understanding Open Chromatin Bias in CUT&RUN and CUT&Tag
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