Related Experiment Video

Updated: Dec 24, 2025

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

11.4K

Selective inhibition of cancer cell self-renewal through a Quisinostat-histone H1.0 axis

Cristina Morales Torres1, Mary Y Wu2, Sebastijan Hobor3

  • 1Cancer Epigenetics Laboratory, Francis Crick Institute, London, NW1 1AT, UK.

Nature Communications
|April 15, 2020
PubMed

Insights

This study reveals that the drug Quisinostat can inhibit cancer cell self-renewal by re-expressing histone H1.0. This approach halts tumor growth and prevents relapse, offering a new strategy for cancer treatment.

Area of Science:

  • Cancer Biology
  • Epigenetics
  • Stem Cell Biology

Background:

  • Cancer growth relies on self-renewing malignant cells.
  • Targeting cancer stem cell self-renewal via signaling pathways is difficult.
  • Epigenetic modifications offer a potential strategy to control cancer cell self-renewal.

Purpose of the Study:

  • To investigate if interfering with the epigenetic state of cancer cells can inhibit their self-renewal.
  • To evaluate the efficacy of Quisinostat in targeting cancer cell self-renewal through histone H1.0 re-expression.
  • To assess Quisinostat's potential in overcoming therapy resistance and preventing cancer relapse.

Main Methods:

  • Investigated the role of histone H1.0 in cancer cell self-renewal.
  • Utilized Quisinostat, a clinically tolerated compound, to induce histone H1.0 re-expression.
  • Assessed the impact of Quisinostat on cancer cell self-renewal, tumor maintenance, and survival of therapy-resistant cells in mouse models.

Main Results:

  • Quisinostat effectively re-expressed histone H1.0, a tumor suppressor.
  • Histone H1.0 re-expression by Quisinostat inhibited cancer cell self-renewal and halted tumor maintenance.
  • Quisinostat hindered the expansion of therapy-surviving cells and reduced disease relapse in lung cancer models, without affecting normal stem cells.

Conclusions:

  • Histone H1.0 is a key mediator of Quisinostat's antitumor effects.
  • Quisinostat selectively targets cancer cell self-renewal by modulating epigenetic state.
  • Sequential administration of targeted therapy and Quisinostat may offer a broadly applicable strategy for prolonged patient response.

More Related Videos

Assays for Validating Histone Acetyltransferase Inhibitors09:11

Assays for Validating Histone Acetyltransferase Inhibitors

Published on: August 6, 2020

6.9K
Global Level Quantification of Histone Post-Translational Modifications in a 3D Cell Culture Model of Hepatic Tissue08:12

Global Level Quantification of Histone Post-Translational Modifications in a 3D Cell Culture Model of Hepatic Tissue

Published on: May 5, 2022

4.3K

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.5K
Multipotency of Hematopoietic Stem Cells01:19

Multipotency of Hematopoietic Stem Cells

The hematopoietic stem cells or HSCs are multipotent, meaning they can differentiate and give rise to all blood and immune cells. HSCs are maintained in the quiescent stage until an external stimulus initiates their differentiation. The multipotent HSCs exist as two heterogeneous populations, long-term repopulating cells (LTRC) and short-term repopulating cells (STRC). The two HSC populations have different surface markers or receptors and are classified based on quiescence and long-term...
3.7K
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
38.1K
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...
5.0K
Histone Variants at the Centromere02:30

Histone Variants at the Centromere

Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
4.9K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.6K