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Related Concept Videos

Eukaryotic Transcription Inhibitors01:52

Eukaryotic Transcription Inhibitors

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Certain biochemical processes, such as embryonic development and cell growth regulation, depend on the repression of specific genes. DNA binding proteins known as eukaryotic transcription inhibitors regulate the repression of gene expression in eukaryotes. The presence of these inhibitors at the required location and time in the cell is triggered by the presence of hormones and additional signals from other cells.
Eukaryotic transcription inhibitors usually contain two distinct domains, a...
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Abnormal Proliferation02:23

Abnormal Proliferation

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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...
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RNA Polymerase II Accessory Proteins02:36

RNA Polymerase II Accessory Proteins

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Proteins that regulate transcription can do so either via direct contact with RNA Polymerase or through indirect interactions facilitated by adaptors, mediators, histone-modifying proteins, and nucleosome remodelers. Direct interactions to activate transcription is seen in bacteria as well as in some eukaryotic genes. In these cases, upstream activation sequences are adjacent to the promoters, and the activator proteins interact directly with the transcriptional machinery. For example, in...
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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

10.0K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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Transcription Factors02:16

Transcription Factors

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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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Related Experiment Video

Updated: Mar 14, 2026

An In Vitro Enzymatic Assay to Measure Transcription Inhibition by GalliumIII and H3 5,10,15-trispentafluorophenylcorroles
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An In Vitro Enzymatic Assay to Measure Transcription Inhibition by GalliumIII and H3 5,10,15-trispentafluorophenylcorroles

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[Inhibiting the pro-tumor and transcription factor FACT: Mechanisms].

N V Maluchenko1,2, H W Chang3, M T Kozinova3

  • 1Biological Faculty, Moscow State University, Moscow, 119234 Russia.

Molekuliarnaia Biologiia
|September 27, 2016
PubMed
Summary

New anticancer drugs called curaxins show promise in eliminating both rapidly growing tumor cells and resistant cancer stem cells (CSCs). Curaxins target multiple molecular pathways crucial for tumor development and reduce CSC populations effectively.

Keywords:
CBL0137FACTNF-κB and HSF1SPT16SSRP1cancer stem cellscuraxinsp53

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Inducible and Reversible Dominant-negative DN Protein Inhibition
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Inducible and Reversible Dominant-negative DN Protein Inhibition

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A Quantitative Assay to Study Protein:DNA Interactions, Discover Transcriptional Regulators of Gene Expression, and Identify Novel Anti-tumor Agents
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A Quantitative Assay to Study Protein:DNA Interactions, Discover Transcriptional Regulators of Gene Expression, and Identify Novel Anti-tumor Agents

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Related Experiment Videos

Last Updated: Mar 14, 2026

An In Vitro Enzymatic Assay to Measure Transcription Inhibition by GalliumIII and H3 5,10,15-trispentafluorophenylcorroles
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An In Vitro Enzymatic Assay to Measure Transcription Inhibition by GalliumIII and H3 5,10,15-trispentafluorophenylcorroles

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Inducible and Reversible Dominant-negative DN Protein Inhibition
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A Quantitative Assay to Study Protein:DNA Interactions, Discover Transcriptional Regulators of Gene Expression, and Identify Novel Anti-tumor Agents
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A Quantitative Assay to Study Protein:DNA Interactions, Discover Transcriptional Regulators of Gene Expression, and Identify Novel Anti-tumor Agents

Published on: August 31, 2013

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cancer stem cells (CSCs) contribute to treatment resistance and poor clinical outcomes.
  • Conventional therapies often fail to eradicate CSCs, highlighting the need for novel therapeutic strategies.
  • CSCs are characterized by slow metabolism and high resistance to existing treatments.

Purpose of the Study:

  • To investigate the efficacy of curaxins, a novel class of compounds, against cancer stem cells (CSCs).
  • To evaluate the impact of curaxins on key molecular pathways involved in tumor progression and CSC survival.
  • To assess the potential of curaxins as a new therapeutic approach for overcoming treatment resistance in cancer.

Main Methods:

  • In vitro and in vivo studies were conducted to assess curaxin activity.
  • Analysis of curaxin's effects on key molecular pathways including p53, NF-κB, and HSF1.
  • Evaluation of curaxin's impact on CSC populations in preclinical cancer models.

Main Results:

  • Curaxins simultaneously target multiple oncogenic molecular cascades (p53, NF-κB, HSF1).
  • Curaxins inhibit genes involved in matrix metalloproteinases, PI3K/AKT/mTOR signaling, and oncogenes like c-MYC.
  • Treatment with curaxin CBL0137 reduced CSC population, contrasting with gemcitabine monotherapy which increased it.

Conclusions:

  • Curaxins demonstrate broad-spectrum antitumor activity by targeting multiple cancer-related pathways.
  • Curaxins effectively reduce cancer stem cell populations, suggesting potential to overcome treatment resistance.
  • Curaxins, particularly FACT inhibitors, represent a promising new class of anticancer drugs with multi-targeted effects.