Department of Anatomy, Korea University College of Medicine, Seoul, Republic of Korea.
Department of Anatomy, Korea University College of Medicine, Seoul, Republic of Korea
Anticancer Res. 2022 Jan;42(1):483-491. doi: 10.21873/anticanres.15506.
BACKGROUND/AIM: Pancreatic cancer is one of the most devastating malignancies worldwide. Because of the disappointing outcome of traditional treatment, new drug candidates are being investigated. This study analysed the effect of eupatilin on pancreatic cancer cells.
Cell viability assay, western blot, siRNA transfection, 2-deoxyglucose uptake assay, AMP/ADP/ATP assay, and fluorescent activated cell sorting were performed.
Eupatilin decreased cell viability and activated AMPK in MIA-PaCa2 cells. Eupatilin decreased glucose uptake in pancreatic cancer, which led to cell starvation and AMPK activation. It is well known that AMPK induces p21 and cell cycle arrest by activating p53. In MIA-PaCa2 cells, p53 is mutated and wild-type p53 protein is suppressed. Treatment with eupatilin induced p21 expression but inhibited the expression of mutated p53. Eupatilin activated Tap73, a p53 family member, which can substitute wild-type p53's role.
Eupatilin shows an anticancer effect against pancreatic cancer cells via glucose uptake inhibition, AMPK activation, and cell cycle arrest.
背景/目的：胰腺癌是全球最具破坏性的恶性肿瘤之一。由于传统治疗的结果令人失望，新的药物候选物正在被研究。本研究分析了泽兰素对胰腺癌细胞的影响。
进行了细胞活力测定、western blot、siRNA 转染、2-脱氧葡萄糖摄取测定、AMP/ADP/ATP 测定和荧光激活细胞分选。
泽兰素降低了 MIA-PaCa2 细胞的活力并激活了 AMPK。泽兰素降低了胰腺癌中的葡萄糖摄取，导致细胞饥饿和 AMPK 激活。众所周知，AMPK 通过激活 p53 诱导 p21 和细胞周期停滞。在 MIA-PaCa2 细胞中，p53 发生突变，野生型 p53 蛋白受到抑制。泽兰素处理诱导了 p21 的表达，但抑制了突变型 p53 的表达。泽兰素激活了 Tap73，一种 p53 家族成员，它可以替代野生型 p53 的作用。
泽兰素通过抑制葡萄糖摄取、激活 AMPK 和诱导细胞周期停滞，对胰腺癌细胞表现出抗癌作用。
