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Review
. 2021 May 12;12(5):723.
doi: 10.3390/genes12050723.

New Insights into the Therapeutic Applications of CRISPR/Cas9 Genome Editing in Breast Cancer

Affiliations
Review

New Insights into the Therapeutic Applications of CRISPR/Cas9 Genome Editing in Breast Cancer

Munazza Ahmed et al. Genes (Basel). .

Abstract

Breast cancer is one of the most prevalent forms of cancer globally and is among the leading causes of death in women. Its heterogenic nature is a result of the involvement of numerous aberrant genes that contribute to the multi-step pathway of tumorigenesis. Despite the fact that several disease-causing mutations have been identified, therapy is often aimed at alleviating symptoms rather than rectifying the mutation in the DNA sequence. The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9 is a groundbreaking tool that is being utilized for the identification and validation of genomic targets bearing tumorigenic potential. CRISPR/Cas9 supersedes its gene-editing predecessors through its unparalleled simplicity, efficiency and affordability. In this review, we provide an overview of the CRISPR/Cas9 mechanism and discuss genes that were edited using this system for the treatment of breast cancer. In addition, we shed light on the delivery methods-both viral and non-viral-that may be used to deliver the system and the barriers associated with each. Overall, the present review provides new insights into the potential therapeutic applications of CRISPR/Cas9 for the advancement of breast cancer treatment.

Keywords: CRISPR; Cas9; breast cancer; metastasis; tumorigenesis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Classification of breast cancer based on histology and molecular features.
Figure 2
Figure 2
An overview of the repair mechanism associated with induced Cas9 double-stranded DNA break. Cleavage is induced by the binding of Cas9- gRNA complex to its complementary sequence on foreign DNA. In eukaryotes, this is amended by either of two mechanisms: the error-prone Non-Homologous End Joining (NHEJ) or Homologous Repair (HR), which is utilized for genome editing by providing a donor template. Created with Biorender.
Figure 3
Figure 3
Reversal of affinities between mutated BRCA1 and 53BP1 towards phosphorylated p53.
Figure 4
Figure 4
The different stages involved in carcinogenesis of breast cancer with respect to some of the contributing genes.

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