Overexpression and knockdown of 5-lipoxygenase regulates the migration and invasion of colorectal cancer cells
- Oncol Lett. 2026 Apr 8;31(6):221. doi: 10.3892/ol.2026.15575.
- 1. Key Laboratory of Research on Human Genetic Diseases at Universities of Inner Mongolia Autonomous Region, Chifeng University, Chifeng, Inner Mongolia Autonomous Region 024000, P.R. China.
- 2. Basic Medicine College, Chifeng University, Chifeng, Inner Mongolia Autonomous Region 024000, P.R. China.
- 3. Department of Endocrinology, Affiliated Hospital of Chifeng University, Chifeng, Inner Mongolia Autonomous Region 024000, P.R. China.
The overexpression of 5-lipoxygenase (5-LOX) plays a notable role in the development of Colorectal Cancer (CRC); however, the specific role of 5-LOX in the migration and invasion of CRC cells through the knockdown and overexpression of 5-LOX has not been well studied. Epithelial-mesenchymal transition (EMT) is associated with an invasive phenotype in CRC; however, the relationship between 5-LOX and EMT in CRC cells remains undefined. In the present study, the effects of 5-LOX overexpression and silencing on migration, invasion and EMT in CRC cells was investigated. In addition, the mRNA levels of vascular endothelial growth factor (VEGF) and angiogenin were also analyzed in human umbilical vein endothelial cells (HUVECs) when co-cultured with media acquired from 5-LOX-silenced or 5-LOX-overexpressed CRC cells. Reverse transcription-quantitative PCR and western blotting analyses were used to determine mRNA and protein expression levels, respectively. Transwell and wound healing assays were used to determine the invasion and migration ability of CRC cells. Fluorescent images were captured to demonstrate the lentiviral Infection in CRC cells. Analysis revealed that the knockdown of 5-LOX by small interfering RNA significantly inhibited migration, invasion and EMT in HCT116 cells, whereas the overexpression of 5-LOX by Recombinant lentiviruses significantly promoted migration, invasion and EMT in RKO cells. Media from 5-LOX-overexpressed RKO cells upregulated the expression of VEGF and angiogenin in HUVECs. These results demonstrated that the overexpression of 5-LOX promoted EMT in CRC cells, which may play a marked role in facilitating cellular migration and invasion. Furthermore, the tumor microenvironment of 5-LOX-overexpressed CRC cells may induce the angiogenesis in HUVECs. The present findings elucidate the role of 5-LOX in the migration and invasion of CRC cells via the knockdown and overexpression of the 5-LOX gene.
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