From: Tumor-derived systems as novel biomedical tools—turning the enemy into an ally
Cancer Cell Line Type | CRISPR Target Gene and Function | Key Findings/Potential Therapeutic Application | Ref |
---|---|---|---|
Murine melanoma B16F10 cell line | • CD47: It acts as a signal on tumor cells to prevent their phagocytosis by macrophages • IL-12: Promotes immune response against tumors by inhibiting angiogenesis, boosting T-cell growth, and inducing TAM polarization | • Tumor cells were genetically engineered to produce IL-12 while simultaneously knocking out the CD47 gene • This dual modification enhanced the immune response by promoting increased macrophage activity | [240] |
Human melanoma cell lines WM115, CM150-Post, and NZM40 | • Early B-cell factor 3 (EBF-3): It acts as a putative epigenetic driver of melanoma metastasis | • DNA methylation editing was conducted, with particular emphasis on the EBF-3 promoter region • Study highlights the promising capabilities of CRISPR for conducting epigenetic editing in disease-related investigations | [241] |
The human NSCLC cell line A549 and the cisplatin-resistant A549 cell line (A549/DDP) | • NNT: It encodes for an enzyme known as nicotinamide nucleotide transhydrogenase, which plays a crucial role in mitochondrial energy metabolism | • CRISPR-based DNA hypermethylation leads to the silencing of NNT in cisplatin-resistant lung cancer cells • Restoring NNT expression reduces resistance to cisplatin and suppresses autophagy | [242] |
ID8 cells (murine ovarian surface epithelial cells) | • Trp53/p53: A crucial tumor suppressor gene that is vital in controlling the cell cycle • Breast cancer susceptibility gene 2: Functions as a tumor suppressor gene, aiding in the prevention of cancer cell formation | • Novel ID8 derivatives were generated by introducing single or double deletions of suppressor genes • This approach enabled the modeling of high-grade serous carcinoma for further study | [243] |
NPC (Nasopharyngeal carcinoma) cell line CNE2 | • KLHDC4: It interacts with tumor suppressor protein p53, thereby augmenting its capacity to initiate apoptosis in cancer cells | • Gene editing of KLHDC4 led to the inhibition of cell proliferation, reduced colony formation, and suppressed tumor growth in mice • Findings suggest KLHDC4 holds promise as a potential therapeutic target and a prognostic biomarker | [244] |
SH-Y5Y neuroblastoma cell line | • Chromosome 6q region: Loss of 6q genetic material, including tumor suppressor CDKN1A, affects cell growth and proliferation and is implicated in neuroblastoma progression • Chromosome 11q region: 11q genetic material loss, including tumor suppressors ATM and CBL, is linked to aggressive neuroblastoma | • CRISPR‒Cas9 mediated deletions in chromosome 11q and 6q revealed oncogenic advantages, suggesting therapeutic potential in targeting these deletions | [245] |
Human cell lines Panc-1 and SUIT-2 and the murine cell line TB32047 | • KrasG12D: It is postulated to be a key driver in tumor initiation and progression | • Three Kras heterozygous cell lines were investigated, and the resulting knockout clones displayed characteristics akin to those of wild-type cells during standard growth conditions | [246] |
Adriamycin-resistant (A2780/ADR) ovarian cancer cell line | • ABCB1: It encodes P-glycoprotein (a membrane protein that aids in the transport of molecules across cell membranes). ABCB1 mutations are associated with anticancer drug resistance | • Downregulation of the ABCB1 results in heightened sensitivity of drug-resistant ovarian cancer cells to doxorubicin treatment | [247] |
PC-9 (lung adenocarcinoma cell line) | • Epidermal growth factor receptor (EGFR): It encodes a protein that governs cell growth, survival, and migration. Abnormalities in this gene can drive cancer growth | • CRISPR/Cas9 introduced EGFR T790M mutation into PC9 lung cancer cells, creating clones resistant to gefitinib but sensitive to AZD9291 | [248] |