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紫檀芪增强人胰腺癌细胞的细胞毒性和化疗敏感性。

Pterostilbene Enhances Cytotoxicity and Chemosensitivity in Human Pancreatic Cancer Cells.

机构信息

Department of Food Science and Biotechnology, National Chung Hsing University, 145 Xingda Road, Taichung 40227, Taiwan.

Department of Forestry, National Chung Hsing University, 145 Xingda Road, Taichung 40227, Taiwan.

出版信息

Biomolecules. 2020 May 4;10(5):709. doi: 10.3390/biom10050709.

DOI:10.3390/biom10050709
PMID:32375296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7281188/
Abstract

Gemcitabine (GEM) drug resistance causes high mortality rates and poor outcomes in pancreatic ductal adenocarcinoma (PDAC) patients. Receptor for advanced glycation end products (RAGE) involvement in the GEM resistance process has been demonstrated. Therefore, finding a safe and effective way to inhibit receptors for RAGE-initiated GEM resistance is urgent. Pterostilbene (PTE), a natural methoxylated analogue derived from resveratrol and found in grapes and blueberries, has diverse bioactivities, such as antioxidative, anti-inflammatory, and anticancer qualities. The overall research objective was to determine the potential of PTE to enhance tumor cytotoxicity and chemosensitivity in PDAC cells. Our results have demonstrated that PTE induced S-phase cell cycle arrest, apoptosis, and autophagic cell death and inhibited multidrug resistance protein 1 (MDR1) expression by downregulating RAGE/PI3K/Akt signaling in both MIA PaCa-2 and MIA PaCa-2 cells (GEM-resistant cells). Remarkably, convincing evidence was established by RAGE small interfering RNA transfection. Taken together, our study demonstrated that PTE promoted chemosensitivity by inhibiting cell proliferation and MDR1 expression via the RAGE/PI3K/Akt axis in PDAC cells. The observations in these experiments indicate that PTE may play a crucial role in MDR1 modulation for PDAC treatment.

摘要

吉西他滨（GEM）耐药导致胰腺导管腺癌（PDAC）患者死亡率高和预后差。已证明晚期糖基化终产物受体（RAGE）参与 GEM 耐药过程。因此，寻找一种安全有效的方法来抑制 RAGE 起始的 GEM 耐药受体是当务之急。紫檀芪（PTE）是一种天然的甲氧基化类似物，来源于白藜芦醇，存在于葡萄和蓝莓中，具有多种生物活性，如抗氧化、抗炎和抗癌特性。总体研究目标是确定 PTE 增强 PDAC 细胞肿瘤细胞毒性和化学敏感性的潜力。我们的研究结果表明，PTE 通过下调 RAGE/PI3K/Akt 信号通路，诱导 MIA PaCa-2 和 MIA PaCa-2 细胞（GEM 耐药细胞）的 S 期细胞周期停滞、凋亡和自噬性细胞死亡，并抑制多药耐药蛋白 1（MDR1）的表达。通过 RAGE 小干扰 RNA 转染，令人信服地证实了这一点。总之，我们的研究表明，PTE 通过抑制 RAGE/PI3K/Akt 轴抑制 PDAC 细胞的增殖和 MDR1 表达，促进化学敏感性。这些实验中的观察结果表明，PTE 可能在 PDAC 治疗中对 MDR1 调节发挥关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/92694623ef0f/biomolecules-10-00709-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/a435349a94af/biomolecules-10-00709-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/f08e98f9c2e8/biomolecules-10-00709-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/7944417ad9e4/biomolecules-10-00709-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/1e7273eb0393/biomolecules-10-00709-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/3b1c5a431b98/biomolecules-10-00709-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/e67b118290fa/biomolecules-10-00709-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/0dc5c5ee3592/biomolecules-10-00709-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/e19a9de55752/biomolecules-10-00709-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/92694623ef0f/biomolecules-10-00709-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/a435349a94af/biomolecules-10-00709-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/f08e98f9c2e8/biomolecules-10-00709-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/7944417ad9e4/biomolecules-10-00709-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/1e7273eb0393/biomolecules-10-00709-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/3b1c5a431b98/biomolecules-10-00709-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/e67b118290fa/biomolecules-10-00709-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/0dc5c5ee3592/biomolecules-10-00709-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/e19a9de55752/biomolecules-10-00709-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6ef/7281188/92694623ef0f/biomolecules-10-00709-g009.jpg

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