Resveratrol induces apoptosis of pancreatic cancers cells by inhibiting miR-21 regulation of BCL-2 expression

Resveratrol induces apoptosis of pancreatic cancers cells by inhibiting miR-21 regulation of BCL-2 expression
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DOI:
10.1007/s12094-012-0999-4
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发表时间:
2013-09-01
影响因子:
3.4
通讯作者:
Tu, Z.
Tu, Z.
中科院分区:
医学4区
文献类型:
--
作者:
Liu, P.;Liang, H.;Tu, Z.

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白藜芦醇是一种可食用的多酚类植物抗毒素,存在于多种植物中,在抑制胰腺癌细胞增殖和诱导凋亡中起重要作用。本文探讨白藜芦醇对PANC-1、CFPAC-1和MIA Paca-2细胞凋亡的作用机制。我们首先用MTT法评估白藜芦醇对PANC-1、CFPAC-1和MIA Paca-2细胞活力的影响。接下来,我们通过实时PCR来评估白藜芦醇对miR-21表达的影响。我们还使用Western blot检测miR-21表达下调后的BCL-2蛋白水平。最后,我们使用miR-21 mimic评估了miR-21对白藜芦醇诱导的抗肿瘤活性的影响。白藜芦醇诱导PANC-1、CFPAC-1和MIA Paca-2细胞活力显著抑制,且呈剂量依赖性。白藜芦醇也能降低miR-21的表达。此外,下调miR-21表达可抑制PANC-1、CFPAC-1和MIA Paca-2细胞中BCL-2的表达。过表达miR-21可逆转白藜芦醇诱导的BCL-2表达下调和细胞凋亡。在本研究中,我们证明了白藜芦醇对细胞凋亡的影响是由于抑制miR-21对BCL-2表达的调节。
Resveratrol is an edible polyphenolic phytoalexin present in different plant species and plays important role in inhibiting proliferation and inducing apoptosis of pancreatic cancer cells. In this paper, the mechanism of resveratrol on PANC-1, CFPAC-1 and MIA Paca-2 cells apoptosis was examined.We first evaluated the effect of resveratrol on viability of PANC-1, CFPAC-1 and MIA Paca-2 cells using MTT assay. Next, we performed real-time PCR to assess the effect of resveratrol on miR-21 expression. We also used Western blot to measure BCL-2 protein levels after down-regulation of miR-21 expression. Finally, we evaluated the effect of miR-21 on resveratrol-induced anti-tumor activity using miR-21 mimic.Resveratrol induced a significant inhibition of PANC-1, CFPAC-1 and MIA Paca-2 cells viability in a dose-dependent manner. Resveratrol also decreased the expression of miR-21. Besides, down-regulation of miR-21 expression can inhibit BCL-2 expression in PANC-1, CFPAC-1 and MIA Paca-2 cells. Over-expression of miR-21 expression can reverse down-regulation of BCL-2 expression and apoptosis induced by resveratrol.In this study, we demonstrated that the effect of resveratrol on apoptosis is due to inhibiting miR-21 regulation of BCL-2 expression.