Smoking promotes the progression of colorectal cancer via CKAP2L/STAT3/AREG/EGFR axis

Smoking is a major risk factor for colorectal cancer (CRC). But the underlying molecular mechanisms by which smoking promotes CRC remain unclear. The positive association between smoking and CRC was confirmed by both cross-sectional study and mendelian randomization analyses. RNA-seq sequencing and bioinformatics analysis were conducted to identify the key genes involved in smoking-induced CRC progression. After treatment with cigarette smoke extract in CRC cells, cell proliferation and metastasis were enhanced. Subsequently, cytoskeleton associated protein 2 like (CKAP2L) was identified as a key gene involved in smoking-induced CRC and its downregulation inhibited cell proliferation and metastasis. CKAP2L is an important part of the cell centrosome and serves a critical role in spindle formation. Previous studies have demonstrated that CKAP2L mediates the cell cycle in a variety of cancer types, promoting the progression and spread of tumors.A recent study reported that regulatory factor X5-regulated CKAP2L can promote the proliferation and metastasis of CRC cells. In this study, we upregulated CKAP2L in HCT116 cells and downregulated CKAP2L in RKO cells. Then, these cells were subjected to the RNA-seq to explore the expression of relative genes. Overall design: RNA sequencing was performed on the negative control RKO cells (RKO-NC), knockdown CKAP2L RKO cells (RKO-shCKAP2L), control HCT116 cells (HCT116-Vector), and overexpression CKAP2L HCT116 cells (HCT116-CKAP2L).