〔Abstract〕 Objective To investigate the effect and mechanism of miR-17 on non-small cell lung cancer(NSCLC) by regulating fatty acid metabolism. Methods The expression of miR-17 mRNA in human non-small cell lung cancer cell lines(H1703, A549, H1299, L78, PGCL3, H460) and normal lung cells(BEAS-2 B) was detected by RT-qPCR. The growth of A549 cells was detected by colony formation assay. The migration ability of A549 cells was detected by scratch test. The invasion ability of A549 cells was detected by Transwell method. The phospholipid and triglyceride content in A549 cells was detected by kit. The expression levels of cluster of differentiation 36(CD36),fatty acid synthase(FASN), acetyl-CoA carboxylase(ACC1) and fatty acid binding protein 5(FABP5) in A549 cells were detected by Western blot. The targeting relationship between miR-17 and stearoyl-CoA desaturase(SCD) was verified by a dual luciferase report. Results In non-small cell lung cancer cell lines(H1703, A549, H1299, L78, PGCL3, H460), the expression of miR-17 mRNA was significantly down-regulated(P<0.01). In the miR-17 mimic group, the number of cell clones significantly decreased(P<0.01), the scratch closure rate significantly decreased(P<0.01), the number of invasive cells significantly decreased(P<0.01), the content of phospholipids and triglycerides significantly decreased(P<0.01), and the expression of FASN, ACC1, FABP5 and CD36 protein was significantly down-regulated(P<0.01). Up regulation of CD36 reversed the regulation of miR-17 on growth, metastasis and fatty acid metabolism in non-small cell lung cancer cells. miR-17 regulated the expression of CD36 by targeting SCD. Conclusion MiR-17 inhibits the growth and metastasis of non-small cell lung cancer cells by targeting SCD to regulate CD36-mediated fatty acid metabolism.