Related Experiment Video
Updated: Jan 7, 2026

06:24
Establishing 3D Endometrial Organoids from the Mouse Uterus
Published on: January 6, 2023
7.5K
Decoding Bromodomain and Extra-Terminal Domain Protein-Mediated Epigenetic Mechanisms in Human Uterine Fibroids
Qiwei Yang1, Somayeh Vafaei1, Ali Falahati2
1Department of Obstetrics and Gynecology, University of Chicago, Chicago, IL 60637, USA.
International Journal of Molecular Sciences
|December 30, 2025
Summary
Bromodomain and extra-terminal domain (BET) proteins are implicated in uterine fibroid (UF) development. Inhibiting BET proteins reduced UF cell growth and altered gene expression, suggesting a potential non-hormonal therapy for uterine fibroids.
Area of Science:
- Gynecology
- Epigenetics
- Molecular Biology
Background:
- Uterine fibroids (UFs) are common benign tumors in women of reproductive age.
- Bromodomain and extra-terminal domain (BET) proteins regulate gene expression but their role in UF pathogenesis is unclear.
Purpose of the Study:
- To investigate BET protein expression in UFs versus myometrium.
- To evaluate the effect of BET inhibitors on UF cell behavior and epigenetics.
Main Methods:
- Compared BET protein levels (BRD2, BRD4) in UF and myometrial tissue.
- Treated UF cells with BET inhibitors (JQ1, I-BET762).
- Assessed cell viability, cell cycle, and performed transcriptomic profiling.
Main Results:
- BET protein expression was altered in UFs.
- BET inhibitors reduced UF cell viability and induced cell cycle arrest.
- Inhibition altered key signaling pathways and reprogrammed the UF epigenome, decreasing extracellular matrix gene expression.
Conclusions:
- BET proteins are crucial regulators in UFs.
- Targeting BET proteins shows promise as a novel, non-hormonal therapeutic strategy for uterine fibroids.
Related Concept Videos
Epigenetic Regulation
3.7K
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...
X-chromosome...
3.7K
Epigenetic Regulation
33.4K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
33.4K
Position-effect Variegation
6.9K
In 1928, a German botanist Emil Heitz observed the moss nuclei with a DNA binding dye. He observed that while some chromatin regions decondense and spread out in the interphase nucleus, others do not. He termed them euchromatin and heterochromatin, respectively. He proposed that the heterochromatin regions reflect a functionally inactive state of the genome. It was later confirmed that heterochromatin is transcriptionally repressed, and euchromatin is transcriptionally active chromatin.
6.9K
Spreading of Chromatin Modifications
9.2K
The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
Writers
The writer...
9.2K
Abnormal Proliferation
5.0K
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...
5.0K
Non-LTR Retrotransposons
13.1K
As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
13.1K

