Table 2 CRISPR/Cas9-mediated target discovery in the immuno-oncology

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]