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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.
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...
Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012 for this...
Genomic Imprinting and Inheritance02:30

Genomic Imprinting and Inheritance

Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...
Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

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Related Experiment Video

Updated: Jun 12, 2026

Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells.

Eduardo F Farias1, Kevin Petrie, Boris Leibovitch

  • 1Department of Medicine, Division of Hematology and Oncology, Tisch Cancer Center, Mount Sinai School of Medicine, New York, NY 10029, USA.

Proceedings of the National Academy of Sciences of the United States of America
|June 16, 2010
PubMed
Summary

Targeting the Sin3A/B paired amphipathic alpha-helices (PAH2) domain with a Sin3 interaction domain (SID) decoy reactivates silenced cancer genes. This epigenetic reprogramming impairs tumor growth and restores drug sensitivity in breast cancer models.

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Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells
09:32

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells

Published on: February 27, 2020

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Last Updated: Jun 12, 2026

Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells
09:32

Differentiation of Mouse Breast Epithelial HC11 and EpH4 Cells

Published on: February 27, 2020

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Molecular Oncology

Background:

  • Sin3A/B proteins are crucial transcriptional corepressors involved in gene silencing and chromatin structure.
  • Aberrant recruitment of Sin3A/B is linked to gene silencing in various cancers.
  • The paired amphipathic alpha-helices (PAH2) domain of Sin3A/B mediates interactions with transcription factors via the Sin3 interaction domain (SID).

Purpose of the Study:

  • To investigate if disrupting the Sin3A/B PAH2 domain function can induce epigenetic reprogramming and gene derepression.
  • To evaluate the therapeutic potential of targeting the PAH2-SID interaction in breast cancer.

Main Methods:

  • Utilized a Sin3 interaction domain (SID) decoy to interfere with PAH2-SID binding in human and mouse breast cancer cells.
  • Assessed the impact of SID decoy on gene expression, epigenetic modifications, and tumor growth in vivo.
  • Tested the efficacy of the SID decoy in triple-negative breast cancer cell lines and its effect on drug sensitivity.

Main Results:

  • Targeted disruption of Sin3A/B function via the SID decoy reversed silencing of genes critical for cell growth and differentiation.
  • The SID decoy induced epigenetic reprogramming and reexpression of E-cadherin, estrogen receptor alpha, and retinoic acid receptor beta.
  • Tumor growth was impaired in vivo, and the SID decoy restored sensitivity to hormonal therapies and retinoids in MDA-MB-231 cells.

Conclusions:

  • Interfering with the PAH2-SID interaction represents a viable epigenetic strategy for breast cancer treatment.
  • Small molecules blocking PAH2-SID interactions could offer a targeted therapeutic approach for breast cancer.
  • This approach may have broader implications for treating cancers driven by aberrant gene silencing.