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Related Concept Videos

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

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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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CRISPR01:59

CRISPR

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Genome editing technologies allow scientists to modify an organism’s DNA via the addition, removal, or rearrangement of genetic material at specific genomic locations. These types of techniques could potentially be used to cure genetic disorders such as hemophilia and sickle cell anemia. One popular and widely used DNA-editing research tool that could lead to safe and effective cures for genetic disorders is the CRISPR-Cas9 system. CRISPR-Cas9 stands for Clustered Regularly Interspaced...
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CRISPR and crRNAs02:53

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Bacteria and archaea are susceptible to viral infections just like eukaryotes; therefore, they have developed a unique adaptive immune system to protect themselves. Clustered regularly interspaced short palindromic repeats and CRISPR-associated proteins (CRISPR-Cas) are present in more than 45% of known bacteria and 90% of known archaea.
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Chromatin Position Affects Gene Expression02:35

Chromatin Position Affects Gene Expression

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Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
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What is Gene Expression?01:42

What is Gene Expression?

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Overview
Gene expression is the process in which DNA directs the synthesis of functional products, that is, proteins. Cells can regulate gene expression at various stages. It allows organisms to generate different cell types and enables cells to adapt to internal and external factors.
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Related Experiment Video

Updated: Jan 30, 2026

Non-Invasive Ultrasound Assessment of Endometrial Cancer Progression in Pax8-Directed Deletion of the Tumor Suppressors Arid1a and Pten in Mice
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Activating PTEN Tumor Suppressor Expression with the CRISPR/dCas9 System.

Colette Moses1, Fiona Nugent2, Charlene Babra Waryah3

  • 1Cancer Epigenetics Laboratory, The Harry Perkins Institute of Medical Research, 6 Verdun Street, Nedlands, WA 6009, Australia; School of Human Sciences, Faculty of Science, The University of Western Australia, 35 Stirling Highway, Perth, WA 6009, Australia.

Molecular Therapy. Nucleic Acids
|January 18, 2019
PubMed
Summary

CRISPR technology can reactivate PTEN expression in aggressive cancers like melanoma and triple-negative breast cancer (TNBC). This targeted PTEN activation inhibits key cancer pathways and improves treatment response.

Keywords:
CRISPR/Cas systemsbreast neoplasmshuman PTEN proteinmelanomatumor suppressor genes

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Overexpressing Long Noncoding RNAs Using Gene-activating CRISPR
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Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • PTEN loss is common in aggressive cancers (melanoma, TNBC), impacting patient prognosis.
  • Mechanisms of PTEN loss include mutation, transcriptional repression, and epigenetic silencing.
  • Transcriptional repression of PTEN can cause resistance to targeted therapies like B-Raf inhibitors.

Purpose of the Study:

  • To investigate the potential of CRISPR-based transcriptional activation of PTEN.
  • To assess if reactivating PTEN can suppress oncogenic signaling and enhance anti-cancer therapy efficacy.

Main Methods:

  • Utilized a CRISPR-dead Cas9 fused to VP64-p65-Rta (dCas9-VPR) transactivator.
  • Directed dCas9-VPR to the PTEN promoter using single-guide RNAs (sgRNAs) in cancer cell lines.
  • Evaluated PTEN expression, downstream signaling pathways (AKT, mTOR, MAPK), and cellular phenotypes (migration, colony formation).

Main Results:

  • dCas9-VPR successfully increased PTEN expression in melanoma and TNBC cells without off-target effects.
  • PTEN activation led to significant repression of AKT, mTOR, and MAPK signaling pathways.
  • In BRAF V600E melanoma cells, dCas9-VPR reduced migration and colony formation, enhancing sensitivity to B-Raf and PI3K/mTOR inhibitors.

Conclusions:

  • CRISPR-mediated PTEN activation is a viable strategy to target aggressive cancers.
  • This approach shows promise for treating cancers resistant to current therapies by restoring PTEN function.