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Article Publish Status: FREE
Abstract Title:

Melittin induces NSCLC apoptosis via inhibition of miR-183.

Abstract Source:

Onco Targets Ther. 2018 ;11:4511-4523. Epub 2018 Aug 1. PMID: 30122943

Abstract Author(s):

Dongqi Gao, Jingjing Zhang, Lu Bai, Fubo Li, Yi Dong, Qingshan Li

Article Affiliation:

Dongqi Gao

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 (2μg/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.

Study Type : Animal Study, In Vitro Study

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Sayer Ji
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