Open AccessPTGS2, CD133, CDK5 knockout comparison by CRISPR CAS-9 system in UV-Induced and Metastatic Melanoma
Author(s) -
Rohan Priyam,
Nicole Guilz,
Allison Cuppia
Publication year - 2021
Publication title -
journal of student research
Language(s) - English
Resource type - Journals
ISSN - 2167-1907
DOI - 10.47611/jsrhs.v10i2.1510
Subject(s) - gene knockdown , melanoma , mmp2 , cancer research , biology , metastasis , mmp9 , gene knockout , conditional gene knockout , knockout mouse , cancer , crispr , phenotype , gene , genetics , downregulation and upregulation
CRISPR Cas9 systems have become an increasingly powerful method to express and repress gene expression. Within cancer research, CRISPR Cas9 technology can be regarded as a tool to knockout or knockin specific genes, ultimately causing metastasis. In this research, the knockout and knockin of the PTGS2, CD133, CDK5 genes are compared to determine whether a knockout or knockin of a specific gene can improve a metastatic melanoma patient’s prognosis. Melanoma is a type of skin cancer with a stage IV survival rate of 22.5%. Several melanoma patients have mutations in the PTGS2, CD133, CDK5 genes, causing metastasis. The knockdown of the PTGS2 gene reduces expression, which inhibits cell proliferation, migration, and invasiveness, modulates immune response by impairing myeloid-derived suppressor cell differentiation, and reduces tumor development and metastasis in vivo. In comparison, the induced knockdown of the CD133 gene results in enhanced invasion and improved MMP2/MMP9 concentrations. MMP2/MMP9 concentrations encode for proteins that degrade type IV collagen, which considers the CD133 gene expression as a key role in tumor growth and metastasis. Lastly, the knockin of CDK5 may be a promising alternative as it controls melanoma cell motility, invasiveness, and metastatic spread.