Drexel University College of Medicine, Philadelphia, PA, USA.
Fox Chase Cancer Center, Philadelphia, PA, USA.
Methods Mol Biol. 2021;2262:323-334. doi: 10.1007/978-1-0716-1190-6_20.
Oncogenic KRAS mutations are common in colorectal cancer (CRC), found in ~50% of tumors, and are associated with poor prognosis and resistance to therapy. There is substantial diversity of KRAS mutations observed in CRC. Importantly, emerging clinical and experimental analysis of relatively common KRAS mutations at amino acids G12, G13, A146, and Q61 suggest that each mutation differently influences the clinical properties of a disease and response to therapy. Although clinical evidence suggests biological differences between mutant KRAS alleles, these differences and the mechanisms underlying them are not well understood, and further exploration of allele-specific differences may provide evidence for individualized therapeutics. One approach to study allelic variation involves the use of isogenic cell lines that express different endogenous KRAS mutants. Here we developed an assay using fluorescent co-selection for CRISPR-driven gene editing to generate various Kras mutations in an isogenic murine colon epithelial cell line background. This assay involves generation of a cell line stably expressing Cas9 linked to BFP and simultaneous introduction of single-guide RNAs (sgRNAs) to two different gene loci resulting in double-editing events. Single-stranded donor oligonucleotides are introduced for a GFP gene and a Kras mutant allele of our choice as templates for homologous recombination (HDR). Cells that successfully undergo HDR are GFP-positive and have a higher probability of containing the desired Kras mutation. Therefore, selection for GFP-positive cells allows us to identify those with phenotypically silent Kras edits. Ultimately, this method allows us to toggle between different mutant alleles and preserve the wild-type allele while maintaining an isogenic background.
致癌性 KRAS 突变在结直肠癌(CRC)中很常见,约占肿瘤的 50%,与预后不良和对治疗的耐药性有关。在 CRC 中观察到 KRAS 突变具有很大的多样性。重要的是,对相对常见的 KRAS 突变氨基酸 G12、G13、A146 和 Q61 的临床和实验分析表明,每种突变都以不同的方式影响疾病的临床特征和对治疗的反应。尽管临床证据表明突变型 KRAS 等位基因之间存在生物学差异,但这些差异及其潜在机制尚未得到很好的理解,进一步探索等位基因特异性差异可能为个体化治疗提供证据。研究等位基因变异的一种方法是使用表达不同内源性 KRAS 突变体的同基因细胞系。在这里,我们开发了一种使用荧光共选择的 CRISPR 驱动基因编辑的测定法,以在同基因鼠结肠上皮细胞系背景中产生各种 Kras 突变。该测定法涉及生成稳定表达 Cas9 与 BFP 连接的细胞系,同时将单引导 RNA(sgRNA)引入两个不同的基因座,导致双编辑事件。单链供体寡核苷酸被引入 GFP 基因和我们选择的 Kras 突变等位基因作为同源重组(HDR)的模板。成功进行 HDR 的细胞是 GFP 阳性的,并且更有可能包含所需的 Kras 突变。因此,选择 GFP 阳性细胞可使我们鉴定那些具有表型沉默 Kras 编辑的细胞。最终,这种方法使我们能够在不同的突变等位基因之间切换,同时保留野生型等位基因并保持同基因背景。