Related Experiment Video

Updated: Dec 26, 2025

A Standard Methodology to Examine On-site Mutagenicity As a Function of Point Mutation Repair Catalyzed by CRISPR/Cas9 and SsODN in Human Cells
10:07

A Standard Methodology to Examine On-site Mutagenicity As a Function of Point Mutation Repair Catalyzed by CRISPR/Cas9 and SsODN in Human Cells

Published on: August 25, 2017

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Kinetics of Nuclear Uptake and Site-Specific DNA Cleavage during CRISPR-Directed Gene Editing in Solid Tumor Cells

Kelly Banas1,2, Natalia Rivera-Torres1, Pawel Bialk1

  • 1Gene Editing Institute, Helen F. Graham Cancer Center and Research Institute, ChristianaCare, Newark, Delaware.

Molecular Cancer Research : MCR
|March 19, 2020
PubMed

Insights

CRISPR gene editing targets cancer by disabling the NRF2 gene in tumor cells. This approach enhances chemosensitivity and lays the groundwork for novel lung cancer therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Editing

Background:

  • Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-directed gene editing is advancing towards clinical use in cancer treatment.
  • Defining the molecular mechanisms, including timing and targeting specificity, is crucial for developing safe and effective CRISPR-based cancer therapies.

Purpose of the Study:

  • To investigate the cellular time frame of CRISPR/Cas complex nuclear entry and gene editing execution.
  • To identify the discrimination mechanism enabling CRISPR/Cas to target tumor cell genomes specifically.
  • To develop CRISPR-directed gene editing for non-small cell lung carcinoma by targeting the Nuclear Factor Erythroid 2-Related Factor-Like (NRF2) gene.

Main Methods:

  • Characterizing the temporal dynamics of CRISPR/Cas nuclear penetration and NRF2 gene disruption.
  • Identifying a unique protospacer adjacent motif for site-specific cleavage of the NRF2 gene in tumor cells.

Main Results:

  • The study defines the time frame for CRISPR-directed gene editing initiation, nuclear penetration, and NRF2 gene disruption.
  • A novel protospacer adjacent motif was identified, enabling specific targeting and cleavage of the NRF2 gene exclusively in tumor genomes.

Conclusions:

  • The findings establish a scientific basis for using CRISPR-directed gene editing as an augmentative therapy for lung cancer.
  • This research supports the potential of CRISPR technology to enhance chemosensitivity and treat solid tumors.

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