miR-21 promotes non-small cell lung cancer cells growth by regulating fatty acid metabolism

• Published in: Cancer cell international Vol. 19; no. 1; p. 219
• Main Authors: Ni, Kewei, Wang, Dimin, Xu, Heyun, Mei, Fuyang, Wu, Changhao, Liu, Zhifang, Zhou, Bing
• Format: Journal Article
• Language: English
• Published: England BioMed Central 23.08.2019; BMC
• Subjects: Apoptosis; CD36; CD36 antigen; Cell growth; Cell migration; Down-regulation; Fatty acid metabolism; Fatty acids; Immunofluorescence; Intracellular; Lipid metabolism; Lipids; Lung cancer; Lungs; Medical prognosis; Metabolism; Metabolites; Metastasis; MicroRNAs; Migration; miR-21; Non-small cell lung cancer cells; Non-small cell lung carcinoma; Phospholipids; Primary Research; Studies; Transfection; Triglycerides; Tumorigenesis; Tumors; China; Cell growth; CD36; miR-21; Fatty acid metabolism; Migration; Non-small cell lung cancer cells
• ISSN: 1475-2867; 1475-2867
• DOI: 10.1186/s12935-019-0941-8

Lung cancer is one of the most common malignant tumors worldwide. CD36 is a receptor for fatty acids and plays an important role in regulating fatty acid metabolism, which is closely related to tumorigenesis and development. The regulation of miR-21 and its role in tumorigenesis have been extensively studied in recent years. However, the relationship between miR-21 and CD36 regulated fatty acid metabolism in human non-small cell lung cancer remains unknown. In this study, lentivirus transfection, qRT-PCR, cell migration, immunofluorescence, and western blot were used to examine the relationship between miR-21 and CD36 regulated fatty acid metabolism and the regulation role of miR-21 in human non-small cell lung cancer. This study demonstrated that up-regulation of miR-21 promoted cell migration and cell growth in human non-small cell lung cancer cells. Moreover, the intracellular contents of lipids including cellular content of phospholipids, neutral lipids content, cellular content of triglycerides were significantly increased following miR-21 mimic treatment compared with control, and the levels of key lipid metabolic enzymes FASN, ACC1 and FABP5 were obviously enhanced in human non-small cell lung cancer cells. Furthermore, down-regulation of CD36 suppressed miR-21 regulated cell growth, migration and intracellular contents of lipids in human non-small cell lung cancer cells, which suggested that miR-21 promoted cell growth and migration of human non-small cell lung cancer cells through CD36 mediated fatty acid metabolism. Inhibition of miR-21 was revealed to inhibit cell growth, migration, intracellular contents of lipids, and CD36 protein expression level in human non-small cell lung cancer cells. In addition, PPARGC1B was a direct target of miR-21, and down-regulation of PPARGC1B reversed the inhibition of CD36 expression induced by miR-21 inhibitor. These results explored the mechanism of miR-21 promoted non-small cell lung cancer and might provide a novel therapeutic method in treating non-small cell lung cancer in clinic.