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Related Concept Videos

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...
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 Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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...
Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...
Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...

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Related Experiment Video

Updated: May 21, 2026

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
10:28

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

Published on: September 20, 2018

HDAC7-Induced Epigenetic Repression Modulates ATF3 Functional Plasticity in Colorectal Cancer Pathogenesis.

Qi Wang1,2,3, Donglei Ji1,2, Yanjie Jia1

  • 1Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, Jilin, 130021, China.

International Journal of Biological Sciences
|May 20, 2026
PubMed
Summary
This summary is machine-generated.

Histone deacetylase 7 (HDAC7) epigenetically silences the tumor suppressor ATF3 in colorectal cancer (CRC). Inhibiting HDAC7 reactivates ATF3, suppressing CRC growth and offering a new therapeutic strategy.

Keywords:
ATF3HDAC7class IIa HDACcolorectal cancerepigenetic repressionscaffold protein

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ATAC-Seq Optimization for Cancer Epigenetics Research
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ATAC-Seq Optimization for Cancer Epigenetics Research

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Assays for Validating Histone Acetyltransferase Inhibitors
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Assays for Validating Histone Acetyltransferase Inhibitors

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Last Updated: May 21, 2026

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
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ATAC-Seq Optimization for Cancer Epigenetics Research
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ATAC-Seq Optimization for Cancer Epigenetics Research

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Assays for Validating Histone Acetyltransferase Inhibitors
09:11

Assays for Validating Histone Acetyltransferase Inhibitors

Published on: August 6, 2020

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Biology

Background:

  • Histone deacetylase 7 (HDAC7) is a Class IIa histone deacetylase implicated in transcriptional regulation.
  • The precise molecular mechanisms of HDAC7 in cancer, particularly colorectal cancer (CRC), are not fully understood.
  • HDAC7's scaffolding functions suggest a role in assembling protein complexes that modify gene expression.

Purpose of the Study:

  • To investigate the role of HDAC7 as an epigenetic regulator in colorectal cancer (CRC).
  • To elucidate the molecular mechanisms by which HDAC7 influences CRC pathogenesis.
  • To evaluate the therapeutic potential of targeting HDAC7 in CRC.

Main Methods:

  • Analysis of HDAC7 expression in CRC tumors and correlation with clinical parameters.
  • Mechanistic studies involving immunoprecipitation and Western blotting to identify protein complexes.
  • Assessment of histone modifications (H3K27ac, H3K18ac) and recruitment of transcription factors (BRD4, RNA polymerase II).
  • Functional assays including genetic depletion and pharmacological inhibition of HDAC7.
  • Cellular assays to evaluate cell cycle arrest, apoptosis, and signaling pathways (PI3K-Akt, Hippo).
  • In vivo studies using xenograft models to assess tumorigenicity.

Main Results:

  • HDAC7 is overexpressed in CRC and associated with advanced stages, metastasis, and poor survival.
  • HDAC7 forms a complex with HDAC3 and ATF3, epigenetically silencing ATF3 transcription by reducing H3K27ac/H3K18ac and blocking BRD4/Pol II recruitment.
  • HDAC7-mediated silencing of ATF3 promotes oncogenic PI3K-Akt signaling and suppresses the Hippo pathway.
  • HDAC7 inhibition or depletion disrupts the repressive complex, leading to ATF3 self-activation.
  • Reactivated ATF3 suppresses CRC proliferation and survival by downregulating Bcl-2, upregulating p21, inducing apoptosis, and inhibiting PI3K-Akt signaling.
  • HDAC7 depletion suppressed tumor growth in vivo xenograft models.

Conclusions:

  • HDAC7 acts as a key epigenetic regulator in CRC by scaffolding a complex that silences the tumor suppressor ATF3.
  • HDAC7 controls ATF3's functional plasticity through competitive cofactor recruitment, switching it from a tumor suppressor to a silenced state.
  • Targeting HDAC7 reactivates ATF3-mediated tumor suppression, presenting a promising therapeutic strategy for CRC.