Table 1.
list of genes that were knocked out using CRISPR/Cas9 technique in different types of cancer and their effects
| Types of Cancer | Target Gene | Cell line | Animal model | Mode of action | Delivery Method | Function | Ref |
|---|---|---|---|---|---|---|---|
| Breast Cancer | P53, PTEN, RB1, NF1 | - | Mice | Knockout | lentiviruses | For both endocrine and chemotherapy, mutated organoids had a greater response rate for mutated organoids. | [47] |
| Breast cancer | miR-23b and miR-27b | MCF7 | Mice | Knockout | lentiviruses | miR-23b and miR-27b have been shown to be oncogenic miRs, and miR-27b reduces tumor development after knockout. | [48] |
| Breast cancer | PTEN, AKT1, PIK3CA | NIH3T3 | Mice | Knockout | lentiviruses |
we show that somatic base editing is feasible and effective at installing defined missense and nonsense mutations at endogenous loci in a mouse model of TNBC. we show that somatic base editing is possible and effective at installing defined missense and nonsense mutations at endogenous loci in a mouse model of TNBC. we show that somatic base editing is feasible and effective at installing defined missense and nonsense mutations at endogenous loci in a mouse model of TNBC. we show that somatic base editing is feasible and effective at installing defined missense and nonsense mutations at endogenous loci in a mouse model of TNBC. we show that somatic base editing is feasible and effective at installing defined missense and nonsense mutations at endogenous loci in a mouse model of TNBC. we show that somatic base editing is feasible and effective at installing defined missense and nonsense mutations at endogenous loci in a mouse model of TNBC. In a TNBC mouse model, somatic base editing may effectively introduce specified missense and nonsense mutations. |
[49] |
| Breast cancer | CBEs | HEK293-T, MDA-MB-231, MCF-7 | - | Knockout | lentiviruses | For ER-driven breast cancer cell growth, unique CTCF-mediated chromatin configurations are required. | [50] |
| Breast cancer | AURKA | HEK293T, MDA-MB-231, SKBR3, MCF7 | - | Knockout | lentiviruses | CHR-6494 might be used in conjunction with MLN8237 to enhance its anti-cancer benefits. | [51] |
| Breast cancer | CXCR4 and CXCR7 | MDA-MB-231 | - | Knockout | lentiviruses | The knockout of CXCR4 and CXCR7 genes reduces the binding ability and activities of CXCL12, slows the growth of TNBC cells, and may be used to treat TNBC. | [52] |
| Breast cancer | PARP1 |
MDA-MB-231, MDA-MB-436 |
- | Knockout | The effectiveness of PARP1 inhibition with chemotherapy for TNBC treatment varies. | [53] | |
| Breast cancer | BRCA1 | MDA-MB-231, ASC | - | Knockdown | lentiCRISPRv2 vector | Breast cancer development is promoted by BRCA1 mutation in the tumor microenvironment. | [54] |
| Breast cancer | APOBEC3G | MCF10A and HCC1806 | - | Knockout | lipofection | multiple clones evaluated for APOBEC3G gene knockout success. | [55] |
| Breast cancer | CDK4, SRPK1, DNMT1 | MCF10A, HEK 293T and GP2-293 | Mice | Knockout | lentiviruses | Transcriptional epistasis influences around 50% of differentially expressed genes in cancer cells. | [56] |
| Breast cancer | CDH1 | MCF-7 | Rats | Knockout | Plasmid Transfection | It is possible to target cancer-related genes using any genome editing technique. | [57] |
| Breast Cancer | OPN | MDA-MB-231 | - | Knockout | CaCl2 transformation | Inactivating osteopontin with CRISPR/Cas9 may overcome radioresistance in breast cancer. | [58] |
| Breast Cancer | BRCA | MDA-MB-231 | - | Knockout | lentivirus | Targeting a group of genes offers new possibilities for PARPi combination treatments. | [59] |
| Breast Cancer | TMEM106A | MDA-MB-231, MDA-MB-468 | - | Knockout | - | In breast cancer, TMEM106A inhibits WDR77 translocation. | [60] |
| Breast and Lung cancer | CDK4, p107, TGFβ1 | A549 and MCF7 | - | Knockout | - | After being challenged with CRISPR cassettes, both cell lines showed a considerable decline in cell count. | [61] |
| Lung cancer | PKP2 | H1299, A549, H460 | - | Knockout | - | Methylation of PKP2 plays an essential factor in radioresistance by stabilizing catenin by CRISPR/Cas9 library screening. | [62] |
| Lung Cancer | Trp53, KRas | HEK-293T | Adult Mice | Knockout | lentiviruses | Using the CRISPR toolset, researchers may rapidly build novel, therapeutically relevant alternative models for biomedical research. | [63] |
| Colon Cancer | KRAS | HT29, WIDR, HCT116, LS174T, and HEK293T; SW480 and A549; and CFPAC-1 | - | Knockout | two-vector lentivirus system | GRB7-PLK1 has a critical axis for RTK tolerance. PLK1 and thus a suitable target for synergizing MEK inhibitors in CRC patients with KRAS mutations. | [64] |
| Colon Cancer | Klotho | Caco-2 | - | Knockout | - | By causing apoptosis, Klotho gene overexpression in Caco-2 cells by CRISPR/Cas9 inhibits cell growth. | [65] |
| Colon cancer | uPAR | CRL1619, CCL247 | - | Knockout | Okayama-Berg vector | Knockout of the uPAR gene Leads to tumor growth inhibition, EGFR downregulation, and an increase in stemness markers. | [66] |
| Prostate cancer | Tceal1 |
Mouse: SP1 Human: PC3M, LNCaP, DU145, CWR22, RWPE |
- | Knockdown | lentivirus | TCEAL1 deletion causes a different cell cycle profile than docetaxel alone, with more subG1 cell death and polyploidy. | [67] |
| Prostate cancer | miRNA (miR)205, miR221, miR222, miR30c, miR224, miR4553, miR23b, miR505 | LNCaP | - | Knockout | Lentivirus | Functional classification of prostate cancer-associated miRNAs through CRISPR/Cas9 mediated gene knockout | [68] |
| Prostate cancer | BRAF | CWR-R1 | - | Knockout | lentiviral | MAPK/AR co-targeting may help patients with active MAPK pathways, especially those with oncogenic BRAF mutations. | [69] |
| Prostate cancer | TP53 | PC-3 | - | Knock-in | lentiviral | The impact of CRISPR/Cas9 guided mutant TP53 gene repair in PC-3 human prostate cancer cells | [70] |
| Prostate cancer | ECE1, ABCA12, BPY2, EEF1A1, RAD9A, and NIPSNAP1 | DU145 and PC3 | - | Knockdown | lentiviral | Prostate cancer metformin Resistance related gene screening using CRISPR-Cas9. | [71] |
| Ovarian cancer | EGFL6 | SKOV3 | - | Knockout | Lentivirus | EGFL6 knockout by CRISPR/Cas9 inhibited tumor angiogenesis. | [72] |
| Ovarian cancer | ZNF587B and SULF1 | A2780, SKOV3, IOSE80 | - | Knockout | Lentivirus | Based on genome-scale CRISPR/Cas9 screening, loss of ZNF587B and SULF1 led to cisplatin resistance. | [73] |
| Ovarian cancer | AR and Nanog expression | A2780, SKOV3 | - | Knock in | Lentivirus | Nanog interaction with androgen receptor signaling axis regulates ovarian cancer stem cells using CRISPR/Cas9. | [74] |
| Ovarian cancer | ITK | SKOV3 | Human | Knockout | Lentivirus | For ovarian cancer metastasis, ITK (IL2 Inducible T Cell Kinase) may be a possible cancer suppressor gene. | [75] |
| thyroid cancer | AXIN1 | ACT-1 | - | Knockout | Viral vector | CRISPR/Cas9 has been used to effectively create an ACT-1 undifferentiated thyroid cancer cell line lacking the AXIN1 gene. | [76] |
| Liver Cancer | PTPMT1 | HCC | - | Knockout and knockdown | lentiCas9-Blast vector | CRISPR-Cas9 knockdown library screening revealed PTPMT1 in the production of cardiolipin as critical to survival in hypoxia in liver cancer. | [77] |
| Liver cancer | Pten, Rb1, and Ctnnb1 | - | Mice | - | px459 V2.0 vector | CRISPR/Cas9-induced Liver cancer mouse model: Longitudinal imaging of liver cancer Using MicroCT and nanoparticle contrasting agents. | [78] |
|
Liver Cancer |
Traf3 | HepG2 | - | Knockout | Lentiviral | The CRISPR/Cas9 method improved HepG2 cell proliferation, migration, and invasion and provided a helpful tool for researching Traf3 function and mechanism. | [79] |
| Liver cancer | ARID1A, | HCC | Pig | Knockout | - | CRISPR/Cas9 editing of pig liver cancer cells to create genetically customized cancer cells. | [80] |