Inhibition of PD-1 protein by the CRISPR-Cas9 method as antitumor therapy of non-small cell lung cancers

Alison Felipe Bordini Biggi; Patricia Ucelli Simioni

doi:10.23925/1984-4840.2019v21i1a2

Autores/as

Alison Felipe Bordini Biggi Faculdade de Americana (FAM), Departamento de Ciências Biomédicas - Americana (SP), Brasil. http://orcid.org/0000-0002-2820-7295
Patricia Ucelli Simioni Faculdade de Americana (FAM), Departamento de Ciências Biomédicas - Americana (SP), Brasil. http://orcid.org/0000-0002-6951-5040

DOI:

https://doi.org/10.23925/1984-4840.2019v21i1a2

Palabras clave:

carcinoma, bronchogenic, CRISPR-Cas Systems, genetic therapy

Resumen

Lung carcinoma is the second most common type of tumor in the world. Among them, 85% of the cases are of non-small cell lung cancer (NSCLC). It is known that, in general, NSCLC tumor cells proliferate due to a reduction in the cytotoxic T lymphocyte response. In the immune response to tumors, the interaction of the programmed death ligand 1 (PD-L1), expressed in tumor cells and the programmed cell death protein 1 (PD-1), expressed in cytotoxic T lymphocytes, promotes suppression of the immune response, leading to inhibition of the activation of cytotoxic T lymphocytes. Despite the biological therapies that have proven effective for the treatment of lung tumors, studies seek a genetic treatment option, such as the CRISPR/Cas9 method. This review aims to provide an update of the CRISPR-Cas9 method and its application as a therapeutic tool in NSCLC to deactivate the gene encoding the PD-1 protein. The genetic alteration of PD-1 protein by CRISPR-Cas9 can affect the interaction between receptor and ligand, allowing cytotoxic T lymphocytes to recognize and exert an antitumor response to NSCLC tumors.

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