Lee Hang-Eun, Choi Eun-Sun, Shin Ji-Ae, Lee Syng-Ook, Park Ki-Soo, Cho Nam-Pyo, Cho Sung-Dae
Department of Oral Pathology, School of Dentistry, Institute of Oral Bioscience, Chonbuk National University, Jeonju 561-756, Republic of Korea.
Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX 77843-4466, USA.
Exp Ther Med. 2014 Jan;7(1):228-232. doi: 10.3892/etm.2013.1368. Epub 2013 Oct 29.
Fucoidan is a sulfated polysaccharide present in brown algae that has been identified to exhibit multiple biological effects. In this study, the apoptotic effects of fucoidan in MC3 human mucoepidermoid carcinoma (MEC) cells were investigated. The apoptotic effects of fucoidan on MC3 MEC cells were evaluated by cell proliferation assay, 4',6-diamidino-2-phenylindole staining and western blot analysis. The results showed that fucoidan decreased cell proliferation and induced caspase-dependent apoptosis in MC3 MEC cells. Fucoidan downregulated the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, whereas phospho-p38 mitogen-activated protein kinase or phospho-c-Jun NH-terminal kinase (JNK) levels were not altered. In addition, fucoidan significantly decreased the expression levels of myeloid cell leukemia-1 (Mcl-1). These results suggest that fucoidan is able to modulate the ERK1/2 pathway and thereby regulate Mcl-1 protein expression and induce apoptosis in MC3 MEC cells. Therefore, fucoidan may be a promising agent for the treatment of human MEC.
岩藻依聚糖是一种存在于褐藻中的硫酸化多糖,已被证实具有多种生物学效应。在本研究中,研究了岩藻依聚糖对MC3人黏液表皮样癌(MEC)细胞的凋亡作用。通过细胞增殖试验、4',6-二脒基-2-苯基吲哚染色和蛋白质印迹分析评估岩藻依聚糖对MC3 MEC细胞的凋亡作用。结果表明,岩藻依聚糖可降低MC3 MEC细胞的增殖并诱导其依赖半胱天冬酶的凋亡。岩藻依聚糖下调细胞外信号调节激酶(ERK)1/2的磷酸化,而磷酸化p38丝裂原活化蛋白激酶或磷酸化c-Jun氨基末端激酶(JNK)水平未改变。此外,岩藻依聚糖显著降低髓样细胞白血病-1(Mcl-1)的表达水平。这些结果表明,岩藻依聚糖能够调节ERK1/2通路,从而调节Mcl-1蛋白表达并诱导MC3 MEC细胞凋亡。因此,岩藻依聚糖可能是治疗人类MEC的一种有前景的药物。