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KMID : 1140220220270040239
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대한암예방학회지
2022 Volume.27 No. 4 p.239 ~ p.246
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Effects of Sangju Honey on Oral Squamous Carcinoma Cells
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Yee Nang-Won
Kim Hyeon-Jin
Kim Eun-Gyung
Cha Yong-Ho
Ma Lei
Cho Na-Eun
Kim Dong-Wook
Kim Chae-Yeon
Kim Sung-Hyun
Ryoo Zae-Young
Yi Jun-Koo
Kim Myoung-Ok
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Abstract
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Since ancient times, honey has been used in traditional medicine owing to its pharmacological effects. It possesses anticancer properties. However, the therapeutic implications of Sangju honey in cancer remains unknown. Therefore, we aimed to demonstrate the potential anticancer effects of Sangju honey on human oral squamous cell carcinoma (OSCC), particularly focusing on epithelial?mesenchymal transition (EMT) and apoptotic and mitogen-activated protein kinase (MAPK) signaling pathways. Ca9-22 and YD-10B human OSCC cells were treated with 0.25% or 0.5% Sangju honey, and the cell viability was examined using the Cell Counting Kit-8 assay. Cell morphology studies were conducted to observe morphological changes, and the wound-healing assay was performed to evaluate the proliferation of honey-treated OSCC cells. Western blot analysis was conducted to investigate protein expression related to EMT and apoptotic and MAPK signaling pathways. Sangju honey reduced cell viability, induced morphological changes, and significantly suppressed the proliferation and migration of Ca9-22 and YD-10B cells. The expression of E-cadherin and N-cadherin was increased and decreased, respectively, in both OSCC cell lines. Moreover, Sangju honey stimulated apoptosis by increasing the expression of p21, p53, cleaved caspase 3, and caspase 9. Furthermore, it downregulated the expression of phospho (p)-extracellular signal-regulated kinases 1 and 2, p-c-Jun amino-terminal kinase, and p-p38 in Ca9-22 and YD-10B cells. Sangju honey inhibits Ca9-22 and YD-10B cell proliferation by regulating EMT, inducing apoptosis, and suppressing the MAPK signaling pathway. Thus, it is a potential anticancer agent for human OSCC.
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KEYWORD
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Sangju honey, Oral squamous cell carcinoma, Cell proliferation, Apoptosis, Mitogen-activated protein kinases
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