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Targeting of the G9a, DNMT1 and UHRF1 epigenetic complex as an effective strategy against pancreatic ductal adenocarcinoma.
J Exp Clin Cancer Res
January 2025
Hepatology Laboratory, Solid Tumors Program, CIMA, CCUN, University of Navarra, Pamplona, Spain.
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with limited treatment options and a poor prognosis. The critical role of epigenetic alterations such as changes in DNA methylation, histones modifications, and chromatin remodeling, in pancreatic tumors progression is becoming increasingly recognized. Moreover, in PDAC these aberrant epigenetic mechanisms can also limit therapy efficacy.
View Article and Find Full Text PDFCrosstalk between non-coding RNAs and programmed cell death in colorectal cancer: implications for targeted therapy.
Epigenetics Chromatin
January 2025
Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran.
Background: Colorectal cancer (CRC) remains one of the most common causes of cancer-related mortality worldwide. Its progression is influenced by complex interactions involving genetic, epigenetic, and environmental factors. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), have been identified as key regulators of gene expression, affecting diverse biological processes, notably programmed cell death (PCD).
View Article and Find Full Text PDFCatalytic-independent functions of the Integrator-PP2A complex (INTAC) confer sensitivity to BET inhibition.
Nat Chem Biol
January 2025
Fudan University Shanghai Cancer Center, Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Medical Epigenetics, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Chromatin and transcription regulators are critical to defining cell identity through shaping epigenetic and transcriptional landscapes, with their misregulation being closely linked to oncogenesis. Pharmacologically targeting these regulators, particularly the transcription-activating BET proteins, has emerged as a promising approach in cancer therapy, yet intrinsic or acquired resistance frequently occurs, with poorly understood mechanisms. Here, using genome-wide CRISPR screens, we find that BET inhibitor efficacy in mediating transcriptional silencing and growth inhibition depends on the auxiliary/arm/tail module of the Integrator-PP2A complex (INTAC), a global regulator of RNA polymerase II pause-release dynamics.
View Article and Find Full Text PDFUnravelling malaria latency: parasite intrinsic and environmental factors influencing dormant liver stages.
Trends Parasitol
January 2025
Department of Molecular Biology, Radboud University, 6525GA, Nijmegen, The Netherlands. Electronic address:
Hypnozoites - dormant Plasmodium parasites in the liver - can cause relapse infections and form a major obstacle to malaria eradication. The mechanisms controlling dormancy remain poorly understood, but hypnozoite formation and reactivation is likely regulated by a combination of parasite intrinsic factors and external stimuli. We reviewed current knowledge of Plasmodium dormancy and drew parallels with dormancy in other parasites and life-cycle stages.
View Article and Find Full Text PDFLiver oval cells in response to HDAC1 inhibitor trichostatin A: immunohistochemical characterization using OV-6 hepatic expression.
Anat Cell Biol
January 2025
Department of Human and Clinical Anatomy, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Sultanate of Oman.
Liver regeneration is intricate, involves many cells, and necessitates extended research. This study aimed to investigate the response of liver oval cells (bipotent liver progenitors) to the epigenetic modifier trichostatin A (TSA), an HDAC1 inhibitor, and to develop a scoring system for assessing the response of these cells. Three groups of equally divided rats (n=24) were selected: control (A, dimethyl sulfoxide treated); oval cell induction (B, acetylaminofluorene [2-AAF] to block hepatocyes/carbon tetrachloride [CCL4] to induce oval cell response); and epigenetic modulation (C, TSA post 2-AAF/CCL4 injury).
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