Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Jun;28(1):295-304.
doi: 10.1007/s40199-019-00240-z. Epub 2019 Jan 21.

CRISPR/Cas9 for overcoming drug resistance in solid tumors

Ali Saber  1 , Bin Liu  1 , Pirooz Ebrahimi  2   3 , Hidde J Haisma  4
Affiliations
Review

CRISPR/Cas9 for overcoming drug resistance in solid tumors

Ali Saber et al. Daru. 2020 Jun.

Abstract

Objectives: In this review, we focus on the application of clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR associated nuclease 9 (Cas9), as a powerful genome editing system, in the identification of resistance mechanisms and in overcoming drug resistance in the most frequent solid tumors.

Data acquisition: Data were collected by conducting systematic searching of scientific English literature using specific keywords such as "cancer", "CRISPR" and related combinations.

Results: The review findings revealed the importance of CRISPR/Cas9 system in understanding drug resistance mechanisms and identification of resistance-related genes such as PBRM1, SLFN11 and ATPE1 in different cancers. We also provided an overview of genes, including RSF1, CDK5, and SGOL1, whose disruption can synergize with the currently available drugs such as paclitaxel and sorafenib.

Conclusion: The data suggest CRISPR/Cas9 system as a useful tool in elucidating the molecular basis of drug resistance and improving clinical outcomes. Graphical abstract The mechanisms of CRISPR/Cas9-mediated genome editing and double-strand breaks (DSBs) repair.

Keywords: CRISPR/Cas9; Clinical outcome; Drug resistance; Drug response; Solid tumor; Targeted therapy.

PubMed Disclaimer

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Graphical abstract
Graphical abstract
The mechanisms of CRISPR/Cas9-mediated genome editing and double-strand breaks (DSBs) repair.
Fig. 1
Fig. 1
The mechanisms of CRISPR/Cas9-mediated genome editing and double-strand breaks (DSBs) repair. CRISPR/Cas9 can introduce DSBs in DNA. The DSBs is repaired by either non-homologous end joining (NHEJ) or homology-directed repair (HDR). Insertions, deletions or other alterations of DNA will occur during this process to achieve gene modifications. PAM: protospacer adjacent motif; sgRNA: single-guide RNA
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Yachida S, Jones S, Bozic I, Antal T, Leary R, Fu B, Kamiyama M, Hruban RH, Eshleman JR, Nowak MA, Velculescu VE, Kinzler KW, Vogelstein B, Iacobuzio-Donahue CA. Distant metastasis occurs late during the genetic evolution of pancreatic cancer. Nature. 2010;467:1114–1117. - PMC - PubMed
    1. Torti D, Trusolino L. Oncogene addiction as a foundational rationale for targeted anti-cancer therapy: promises and perils. EMBO Mol Med. 2011;3:623–636. - PMC - PubMed
    1. van der Wekken AJ, Saber A, Hiltermann TJN, Kok K, van den Berg A, Groen HJM. Resistance mechanisms after tyrosine kinase inhibitors afatinib and crizotinib in non-small cell lung cancer, a review of the literature. Crit Rev Oncol Hematol. 2016;100:107–116. - PubMed
    1. Saber A, Van Der Wekken AJ, Kok K, Terpstra MM, Bosman LJ, Mastik MF, et al. Genomic aberrations in crizotinib resistant lung adenocarcinoma samples identified by transcriptome sequencing. PLoS One. 2016;11(4):e0153065. - PMC - PubMed
    1. Saber A, van der Wekken A, Hiltermann TJN, Kok K, van den Berg A, Groen HJM. Genomic aberrations guiding treatment of non-small cell lung cancer patients. Cancer Treat Commun. 2015;4:23–33.

Substances

LinkOut - more resources