From: CRISPR/Cas9 system: recent applications in immuno-oncology and cancer immunotherapy
Location | Target | Biological function | Genome-editing technology | Effects after CRISPR-engineering | Reference |
---|---|---|---|---|---|
Tumor cell | PTPN2 | A phosphate mediating IFN-γ sensing | CRISPR-KO | PTPN2 KO increases antigen presentation and anti-tumor toxicity. | [36] |
ASAF1 | A regulator of drug-sensitivity | CRISPR-KO | ASAF1 KO prompts M1-type macrophage polarization and potentiates T-cell activation | [35] | |
Cop1 | A modulator recruiting M2-type macrophage | CRISPR-KO | Cop1 KO decreases immune escape and enhances ICI efficacy | [36] | |
KEAP1 | Drug-resistance gene | CRISPR-KO | KEAP1 KO allows tumor cells to proliferate without MAPK signaling. | [57] | |
Immune cell | REGNASE1 | Metabolism-related gene | CRISPR-KO | REGNASE1 KO enhances the accumulation of tumor-specific T-cell | [58] |
CARM1 | Epigenetic enzyme | CRISPR-KO | CARM1 KO enhances anti-tumor immunity and sensitizes resistant tumors to ICI | [59] | |
FLI1 | Transcription factor | CRISPR-KO | CD8 + T-cells deleting Fli1 exert a more protective immunity. | [60] | |
CBAF and INO80 complex | A regulator of T-cell exhaustion | CRISPR-KO | CBAF and INO80 complex KO prolongs T-cell persistence. | [61] | |
FAM49B | Negative regulators of T-cell response | CRISPR-KO | FAM49B KO prompts T-cell activation. | [62] | |
Tumor-immune interaction | PRC2 | A negative regulator of IFN-γ-induced MHC-1 expression | CRISPR-KO | PRC2 KO upregulates MHC-1 expression and enhance tumor recognition by immune cells. | [63] |
CMTM6 | A positive regulator of IFN-γ-induced PD-L1 expression | CRISPR-KO | CMTM6 KO downregulates PD-L1 expression. | [64] | |
TRAF3 | A negative regulator for MHC-1 expression | CRISPR-KO | TRAF KO upregulates MHC-1 expression. | [65] | |
SIGLEC | Glycan-binding immune receptor | CRISPR-KO | Blocking CD34-SIGLEC7 interplay makes tumor cells more vulnerable to immune cell attack. | [66] |