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Year : 2014  |  Volume : 10  |  Issue : 1  |  Page : 43-49

Anti-cancer Effects of CME-1, a Novel Polysaccharide, Purified from the Mycelia of Cordyceps sinensis against B16-F10 Melanoma Cells

1 Department of Pharmacology and Graduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan
2 Department of Surgery, Chi-Mei Medical Center, Tainan, Taiwan
3 Core Facility Center, Office of Research and Development, Taipei, Taiwan
4 School of Oral Hygiene, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan

Correspondence Address:
Joen-Rong Sheu
Department of Pharmacology, Graduate Institute of Medical Sciences, Taipei Medical University, 250 Wu-Hsing St., Taipei 110
Yung-Kai Huang
School of Oral Hygiene, College of Oral Medicine, Taipei Medical University, Taipei 110
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Source of Support: National Science Council, Taiwan (NSC97-2320- B-038-016-MY3 and NSC100-2320-B-038-021-MY3); Chi-Mei Medical Center-Taipei Medical University (101CM-TMU-07), Conflict of Interest: None

DOI: 10.4103/0973-1482.131365

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Background: Matrix metalloproteinases (MMPs) play important roles in the invasion and migration of cancer cells. In melanoma, several signaling pathways are constitutively activated. Among these, the mitogen-activated protein kinase (MAPKs) signaling pathways are activated through multiple signal transduction molecules and appear to play major roles in melanoma progression. Therefore, the inhibition of MAPK signaling might be a crucial role for the treatment of melanoma cancer. Aims: We examined the anticancer effect of CME-1, a novel water-soluble polysaccharide fraction, isolated from Cordyceps sinensis mycelia on B16-F10 melanoma cells. Materials and Methods: B16-F10 cells were exposed to different concentrations of CME-1 (250, 500 and 800 μg/ml) for 24 h in 5% CO 2 incubator at 37°C. Western blot analysis was performed to detect the expression of MMP-1, p-p38 MAPK, p-ERK1/2, and IkB-α in B16-F10 cells. Cell migration test was performed by wound healing migration assay. Results: CME-1 suppresses cell migration in a concentration-dependent manner. Western blotting analysis revealed that CME-1 led to the reduction on the expression levels of MMP-1 and down regulated the expression of phosphorylated extracellular signal-regulated kinase (ERK1/2 and p38 mitogen-activated protein kinase (p38 MAPK). CME-1 restored the IkB-degradation in B16F10 cells. Conclusions: These results indicate that CME-1 inhibited MMP-1 expressions in B16F10 melanoma cells through either NF-kB or ERK/p38 MAPK down regulation thereby inhibiting B16F10 cell migration. Therefore, we proposed that CME-1 might be developed as a therapeutic potential candidate for the treatment of cancer metastasis.

Abstract in Chinese

CME-1的抗肿瘤效果,一种从虫草中提取的新多聚糖对抗B16-F10恶性黑色素瘤细胞 背景:间质金属蛋白酶(MMPs)在肿瘤细胞的侵袭和转移中起重要作用。在恶性黑色素瘤中,数条信号通路组成性激活。其中,细胞分裂素活化蛋白激酶(MAPKs)信号通路通过多种单信号转导分子激活并起主要作用。因此抑制MAPK信号通路可能在治疗恶黑中起关键作用。 目的:我们检验了CME-1对B16-F10恶性黑色素瘤细胞的抗癌作用,CME-1是一种新型水溶性多聚糖片段,从虫草菌丝中分离提取。 材料和方法:B16-F10恶性黑色素瘤细胞暴露于不同浓度的CME-1中(250,500和800μg/ml),在5% CO2浓度37°C恒温下24小时。蛋白印迹分析用来检测MMP-1,p-p38 MAPK, p-ERK1/2,和IkB-α在 B16-F10细胞中的表达。细胞迁移试验通过伤口愈合迁移试验来实施。 结果:在浓度相关的前提下,CME-1抑制细胞迁移。蛋白印迹分析显示CME-1导致MMP-1表达水平的降低,下调磷酸化细胞外信号调节激酶(ERK1/2)和p38有丝分裂活性蛋白激酶(p38 MAPK)。CME-1修复了B16F10细胞中的IKB降解。 结论:结果表明CME-1通过下调NF-kB或 ERK/p38MAPK抑制B16F10恶黑细胞中的MMP-1表达,因而抑制B16F10细胞转移。因此,我们建议将CME-1作为治疗恶性黑色素瘤的手段之一。 关键词:细胞迁移,CME-1, ERK/p38MAPK, 恶性黑色素瘤, MMP-1

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