Effect of depletion of CYP4F11 on proliferation and migration in lung cancer cell lines NCI-H460 cell line.
Lung cancer remains the leading cause of cancer deaths worldwide. Drug resistance in lung cancer patients often limits treatment effectiveness, underscoring the need for novel therapeutic targets. In our recent work, we identified the cytochrome P450 4F11 (CYP4F11) as a promising therapeutic target for lung cancer. CYP4F11 belongs to the CYP4F family of fatty acid omega-hydroxylases catalyzing the conversion of arachidonic acid to the potent lipid mediator 20-hydroxyeicosatetraenoic acid (20-HETE). 20-HETE is a long-known key player in cancer cell proliferation and migration. CYP4F11 is highly overexpressed in patients with lung cancer. Through genetic modification studies in lung cancer cell lines, we found that CYP4F11 indeed mediates the proliferation and migration through 20-HETE production. However, it is currently unknown how CYP4F11 contributes to lung cancer progression and what the underlying mechanism is. Our data identify differentially expressed genes in CYP4F11-knockdown lung cancer cells compared to control cells via RNA sequencing. We provide better understanding on the cellular mechanism involving CYP4F11 in lung cancer. Overall design: RNA-seq profiling of wildtype NCI-H469 cells and ther knockdown derivatives (siCYP4F11) 24h post transfection.