Related Experiment Video

Updated: May 13, 2026

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
06:07

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

Curcumin down-regulates DNA methyltransferase 1 and plays an anti-leukemic role in acute myeloid leukemia

Jianhua Yu1, Yong Peng, Lai-Chu Wu

  • 1Division of Hematology, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America. Jianhua.yu@osumc.edu

Plos One
|March 5, 2013
PubMed

Insights

Curcumin, a compound in turmeric, may treat acute myeloid leukemia (AML) by down-regulating DNMT1, reactivating tumor suppressor genes, and inducing cancer cell death. This dietary supplement shows promise for AML therapy.

Area of Science:

  • Oncology
  • Epigenetics
  • Pharmacology

Background:

  • DNA methylation is crucial in acute myeloid leukemia (AML) development.
  • Curcumin, from turmeric, is a bioactive compound with potential anti-cancer properties.
  • The role of curcumin in AML epigenetics, specifically DNA hypomethylation, is largely unexplored.

Purpose of the Study:

  • To investigate the effect of curcumin on DNA methylation in AML.
  • To elucidate the mechanism by which curcumin influences DNA methyltransferase 1 (DNMT1) expression.
  • To evaluate curcumin's therapeutic potential in AML models.

Main Methods:

  • Curcumin treatment of AML cell lines (in vitro) and primary AML cells (ex vivo).
  • Analysis of DNMT1 expression and its regulators (p65, Sp1) using molecular assays.
  • Assessment of tumor suppressor gene (p15INK4B) methylation and expression.
  • Evaluation of cell cycle arrest and apoptosis induction.
  • In vivo studies using mouse models of AML.

Main Results:

  • Curcumin down-regulated DNMT1 expression in AML cells.
  • Curcumin reduced p65 and Sp1 expression, decreasing their binding to the DNMT1 promoter.
  • Curcumin reactivated the p15INK4B tumor suppressor gene via promoter hypomethylation.
  • Curcumin induced G1 cell cycle arrest and apoptosis in AML cells.
  • Curcumin suppressed AML tumor growth in vivo.

Conclusions:

  • Curcumin demonstrates potential as a therapeutic agent for AML by targeting DNMT1 and epigenetic modifications.
  • The mechanism involves down-regulation of DNMT1 through key transcription factors, leading to tumor suppressor gene reactivation.
  • Curcumin warrants further investigation as a single agent or adjuvant therapy for AML treatment.

More Related Videos

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients13:21

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

Published on: June 16, 2017

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...