金聖草素作為治療癌症藥物之可行性評估

在前列腺癌機制中雄激素受體和信號轉導及轉錄激活蛋白3的持續性活化在前列腺癌進展起到重要地位。目前對前列腺癌的治療主要方向在針對雄激素受體阻斷，但進展到晚期經常會轉變為雄激素不敏感的去勢療法無效前列腺癌。金聖草素屬於多酚類物質下的黃酮類物質，許多黃酮類物質可在生物體內互相轉換。金聖草素為許多草本植物的萃取物的成分之一，已展現出一些抗氧化和抑制癌細胞體外生長並使之凋亡的特性，故以金聖草素測試對前列腺癌細胞株的影響。藉由細胞活性試驗和凋亡試驗已確定金聖草素會抑制LNCaP細胞活性和使其凋亡，藉由Western blot實驗已確定會使p-STAT 3和Bcl-2表現下降，Active-Caspase 3和Cleaved-PARP則表現上升，藉由活性氧物質實驗也確定經過金聖草素處理細胞ROS會增加，以上結果顯示抑制STAT 3路徑和增加ROS共同參與了細胞凋亡。本研究認為金聖草素可成為有潛力的前列腺癌藥物。

Androgen receptor and STAT3 play an important role in prostate cancer mechanism. Up to now, the treatment of prostate cancer mainly focus on androgen receptor blockage. But this cancer usually tends to Castration-resistant prostate cancer in late stage. Chrysoeriol belongs to polyphenol. It is a kind of flavon material. Many flavones could transfer each other in vivo. Chrysoeriol is an ingredient of many herbal extracts, it has shown some anti-oxidant and anti-tumor characters. In this study, we used chrysoeriol to treat LNCaP cell line. It is obviously chrysoeriol could inbibit LNCaP and induce apoptosis by cell viability and apoptosis experiment. Furthermore, we observed Active-Caspase3 and Cleaved-PARP upregulated by western blot. In contrast, p-STAT3 and Bcl-2 are downregulated. Besides, ROS level arised after treatment. This result shows that STAT3 inhibition and ROS rising cooperate in the apoptosis of LNCaP, we conclude that chrysoeriol could be a potential anticancer medicine.