%0 Journal Article %T Melittin Induced G1 Cell Cycle Arrest and Apoptosis in Chago-K1 Human Bronchogenic Carcinoma Cells and Inhibited the Differentiation of THP-1 Cells into Tumour- Associated Macrophages %J Asian Pacific Journal of Cancer Prevention %I West Asia Organization for Cancer Prevention (WAOCP), APOCP's West Asia Chapter. %Z 1513-7368 %A Tipgomut, Chartsiam %A Wongprommoon, Arin %A Takeo, Emi %A Ittiudomrak, Teeranai %A Puthong, Songchan %A Chanchao, Chanpen %D 2018 %\ 12/01/2018 %V 19 %N 12 %P 3427-3434 %! Melittin Induced G1 Cell Cycle Arrest and Apoptosis in Chago-K1 Human Bronchogenic Carcinoma Cells and Inhibited the Differentiation of THP-1 Cells into Tumour- Associated Macrophages %K Apoptosis %K bronchogenic carcinoma %K melittin %K tumor-associated macrophage %K cathepsin S %R 10.31557/APJCP.2018.19.12.3427 %X Background: Bronchogenic carcinoma (lung cancer) is one of the leading causes of death. Although manycompounds isolated from natural products have been used to treat it, drug resistance is a serious problem, and alternativeanti-cancer drugs are required. Here, melittin from Apis mellifera venom was used, and its effects on bronchogeniccarcinoma cell proliferation and tumour-associated macrophage differentiation were evaluated. Methods: The halfmaximal inhibitory concentration (IC50) of melittin was measured by MTT. Cell death was observed by annexin Vand propidium iodide (PI) co-staining followed by flow cytometry. Cell cycle arrest was revealed by PI staining andflow cytometry. To investigate the tumour microenvironment, differentiation of circulating monocytes (THP-1) intotumour-associated macrophages (TAMs) was assayed by sandwich-ELISA and interleukin (IL)-10 levels were determined.Cell proliferation and migration was observed by flat plate colony formation. Secretion of vascular endothelial growthfactor (VEGF) was detected by ELISA. The change in expression levels of CatS, Bcl-2, and MADD was measured byquantitative RT-PCR. Results: Melittin was significantly more cytotoxic (p < 0.01) to human bronchogenic carcinomacells (ChaGo-K1) than to the control human lung fibroblasts (Wi-38) cells. At 2.5 μM, melittin caused ChaGo-K1cells to undergo apoptosis and cell cycle arrest at the G1 phase. The IL-10 levels showed that melittin significantlyinhibited the differentiation of THP-1 cells into TAMs (p < 0.05) and reduced the number of colonies formed in thetreated ChaGo-K1 cells compared to the untreated cells. However, melittin did not affect angiogenesis in ChaGo-K1cells. Unlike MADD, Bcl-2 was up-regulated significantly (p < 0.05) in melittin-treated ChaGo-K1 cells. Conclusion:Melittin can be used as an alternative agent for lung cancer treatment because of its cytotoxicity against ChaGo-K1cells and the inhibition of differentiation of THP-1 cells into TAMs. %U https://journal.waocp.org/article_77406_47ba9fcd1fa1734bb148764f50eb9529.pdf