CRISPR/Cas9 and cancer targets: future possibilities and present challenges.

Martyn K White,Kamel Khalili

doi:10.18632/oncotarget.7104

Abstract

All cancers have multiple mutations that can largely be grouped into certain classes depending on the function of the gene in which they lie and these include oncogenic changes that enhance cellular proliferation, loss of function of tumor suppressors that regulate cell growth potential and induction of metabolic enzymes that confer resistance to chemotherapeutic agents. Thus the ability to correct such mutations is an important goal in cancer treatment. Recent research has led to the developments of reagents which specifically target nucleotide sequences within the cellular genome and these have a huge potential for expanding our anticancer armamentarium. One such a reagent is the clustered regulatory interspaced short palindromic repeat (CRISPR)-associated 9 (Cas9) system, a powerful, highly specific and adaptable tool that provides unparalleled control for editing the cellular genome. In this short review, we discuss the potential of CRISPR/Cas9 against human cancers and the current difficulties in translating this for novel therapeutic approaches.

Highlights

Since all cancers contain multiple mutations that allow them to grow progressively and exhibit the characteristics of malignancy [1, 2], targeting the cancer cell genome is an attractive approach
We discuss the potential of clustered regulatory interspaced short palindromic repeat (CRISPR)/Cas9 against human cancers and the current difficulties in translating this for novel therapeutic approaches
As well as viral tumor suppressor inactivating proteins, tumor suppressors can become inactivated by mutations in their cellular genes and these have a huge potential as targets for treating human cancer www.impactjournals.com/oncotarget by correcting them with CRISPR/Cas9

Summary

Introduction

Since all cancers contain multiple mutations that allow them to grow progressively and exhibit the characteristics of malignancy [1, 2], targeting the cancer cell genome is an attractive approach. All cancers have multiple mutations that can largely be grouped into certain classes depending on the function of the gene in which they lie and these include oncogenic changes that enhance cellular proliferation, loss of function of tumor suppressors that regulate cell growth potential and induction of metabolic enzymes that confer resistance to chemotherapeutic agents. Other viruses express oncogenes that are associated with human cancer and are potential targets for CRISPR/ Cas9.

Results

Conclusion