1. Melittin induces NSCLC apoptosis via inhibition of miR-183.
- Author
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Gao, Dongqi, Zhang, Jingjing, Bai, Lu, Li, Fubo, Dong, Yi, and Li, Qingshan
- Subjects
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NON-small-cell lung carcinoma , *MELITTIN , *PROGNOSIS , *ANTI-inflammatory agents , *FLOW cytometry - Abstract
Background: Non-small-cell lung cancer (NSCLC) has one of the highest mortality rates among cancers worldwide, with a poor prognosis. Previous studies have reported that melittin, an active component of apitoxin, exerts anti-inflammatory and antitumor effects via vascular endothelial growth factor or FoxO1. Methods: CCK8, flow cytometry assay and Western blotting were performed to evaluate the effect of melittin on NSCLC. Results: The present study demonstrates that melittin activated caspase-2 by inhibiting miR-183 expression and, thus, induced NSCLC apoptosis in both NCI-H441 cancer cell line assays and an in vivo xenograft model. The results of the cell-based assays showed that melittin (2 µg/mL) robustly suppressed miR-183 expression level and resulted in decreased invasion and migration abilities of NCI-H441 cells. Additionally, a flow cytometry assay and Western blotting showed that melittin induced NSCLC NCI-H441 cell apoptosis along with significant elevation of caspase-2 and Bax, which are regulators of cell apoptosis, and reduced Bcl-2 protein expression compared with dimethyl sulfoxide control. Furthermore, subcutaneous injection of melittin (5 mg/kg) significantly suppressed NSCLC tumor growth compared with vehicle group tumors, determined through tumor size and weight. Conclusion: Taken together, the aforementioned findings contribute to identification of a novel therapeutic target in the treatment of NSCLC, in patients diagnosed with a high expression of miR-183. Moreover, this article provides solid evidence for the inhibitory effect of melittin on NSCLC cancer cell growth. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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