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Abstract：
BACKGROUND: In Korea and China, asiasari radix (AR) is widely used as a traditional anti-inflammatory and analgesic agent. After its skin-regenerating and hair loss-preventing activities were identified, several types of AR extracts were used for aesthetic purposes. Nevertheless, the effect of ARE on various types of skin cancers was not fully studied yet.
METHODS: In this study, we tested the effect of an ethanolic AR extract (ARE) on G361 human melanoma and HaCaT human keratinocyte cell lines. After ARE exposure, cell growth and the expression patterns of proteins and genes were monitored.
RESULTS: The ARE-mediated cell growth inhibition was greater in G361 cells than in HaCaT cells due to differences in its cell growth regulation effects. Interestingly, ARE treatment induced caspase-3-mediated apoptosis in G361 cells, but not in HaCaT cells. Furthermore, ARE reduced the expression of p53 and p21 proteins in G361 cells, whereas it induced their expression in HaCaT cells. ARE induced cell death in G361 cells through the reactive oxygen species (ROS)-dependent regulation of p53 and p21 in G361 cells. Microarray analysis showed that ARE regulates Mouse double minute 2 homolog (MDM2) and CASP8 and FADD-like apoptosis regulator (CFLAR) gene expression in G361 and HaCaT cells differently.
CONCLUSIONS: The treatment of ARE preferentially induces apoptosis in melanoma cells by the ROS-dependent differential regulation of p53 level. Therefore, ARE can be used as a new medicinal option for melanoma.
METHODS: In this study, we tested the effect of an ethanolic AR extract (ARE) on G361 human melanoma and HaCaT human keratinocyte cell lines. After ARE exposure, cell growth and the expression patterns of proteins and genes were monitored.
RESULTS: The ARE-mediated cell growth inhibition was greater in G361 cells than in HaCaT cells due to differences in its cell growth regulation effects. Interestingly, ARE treatment induced caspase-3-mediated apoptosis in G361 cells, but not in HaCaT cells. Furthermore, ARE reduced the expression of p53 and p21 proteins in G361 cells, whereas it induced their expression in HaCaT cells. ARE induced cell death in G361 cells through the reactive oxygen species (ROS)-dependent regulation of p53 and p21 in G361 cells. Microarray analysis showed that ARE regulates Mouse double minute 2 homolog (MDM2) and CASP8 and FADD-like apoptosis regulator (CFLAR) gene expression in G361 and HaCaT cells differently.
CONCLUSIONS: The treatment of ARE preferentially induces apoptosis in melanoma cells by the ROS-dependent differential regulation of p53 level. Therefore, ARE can be used as a new medicinal option for melanoma.
摘要：
背景：在韩国和中国，asasariradix（AR）被广泛用作传统的抗炎和镇痛药。在确定其皮肤再生和防止脱发的活动后，几种类型的AR提取物用于美学目的。然而，ARE对各种类型皮肤癌的影响尚未得到充分研究.
方法：在本研究中，我们测试了乙醇AR提取物（ARE）对G361人黑色素瘤和HaCaT人角质形成细胞系的影响。暴露后，监测细胞生长以及蛋白质和基因的表达模式。
结果：由于其细胞生长调节作用的差异，ARE介导的细胞生长抑制在G361细胞中比在HaCaT细胞中更大。有趣的是,ARE处理诱导的caspase-3介导的G361细胞凋亡，但不是在HaCaT细胞中.此外，ARE降低了G361细胞中p53和p21蛋白的表达，而它诱导它们在HaCaT细胞中的表达。ARE通过G361细胞中p53和p21的活性氧（ROS）依赖性调节诱导G361细胞死亡。微阵列分析表明，ARE在G361和HaCaT细胞中不同程度地调节小鼠双分2同源物（MDM2）和CASP8和FADD样凋亡调节因子（CFLAR）基因的表达。
结论：ARE的治疗通过ROS依赖性的p53水平差异调节优先诱导黑色素瘤细胞凋亡。因此,ARE可以用作黑色素瘤的新药物选择。
方法：在本研究中，我们测试了乙醇AR提取物（ARE）对G361人黑色素瘤和HaCaT人角质形成细胞系的影响。暴露后，监测细胞生长以及蛋白质和基因的表达模式。
结果：由于其细胞生长调节作用的差异，ARE介导的细胞生长抑制在G361细胞中比在HaCaT细胞中更大。有趣的是,ARE处理诱导的caspase-3介导的G361细胞凋亡，但不是在HaCaT细胞中.此外，ARE降低了G361细胞中p53和p21蛋白的表达，而它诱导它们在HaCaT细胞中的表达。ARE通过G361细胞中p53和p21的活性氧（ROS）依赖性调节诱导G361细胞死亡。微阵列分析表明，ARE在G361和HaCaT细胞中不同程度地调节小鼠双分2同源物（MDM2）和CASP8和FADD样凋亡调节因子（CFLAR）基因的表达。
结论：ARE的治疗通过ROS依赖性的p53水平差异调节优先诱导黑色素瘤细胞凋亡。因此,ARE可以用作黑色素瘤的新药物选择。
