| 描述信息 |
Colorectal cancer (CRC) is a leading cause of cancer-related deaths globally and one of the most common digestive tumors. While non-coding genomic variations and epigenetic modifications are increasingly linked to CRC pathogenesis, their effects on enhancer activity remain largely unexplored. In this study, we developed and applied two high-throughput techniques, SNP-STARR-seq and Methyl-STARR-seq, to systematically evaluate the influence of 30,790 non-coding single nucleotide polymorphisms (SNPs) and over 134,000 CpG sites on enhancer activity in cells sourced from primary and metastatic colorectal cancer (CRC). Additionally, we generated two independent knockout (KO) HCT116 cell lines using CRISPR/Cas9, each with a short fragment (89 bp and 136 bp, respectively) spanning the target SNP rs6061231 removed from the genome. |
