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厚朴酚抑制胰腺癌发展并负向调节TGF-β/Smad信号通路。

Magnolol Suppresses Pancreatic Cancer Development and Negatively Regulating TGF-β/Smad Signaling.

作者信息

Chen Shuo, Shen Jiaqi, Zhao Jing, Wang Jiazhong, Shan Tao, Li Junhui, Xu Meng, Chen Xi, Liu Yang, Cao Gang

机构信息

Department of General Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an Jiaotong University, Xi'an, China.

School of Life Science, Xiamen University, Xiamen, China.

出版信息

Front Oncol. 2020 Dec 2;10:597672. doi: 10.3389/fonc.2020.597672. eCollection 2020.

DOI:10.3389/fonc.2020.597672
PMID:33344246
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7738609/
Abstract

Magnolol, a hydroxylated biphenyl extracted from , has recently drawn attention due to its anticancer potential. The present study was aimed to explore the effects of Magnolol on restraining the proliferation, migration and invasion of pancreatic cancer and . Magnolol showed significant anti-growth effect in an orthotopic xenograft nude mouse model, and immunohistochemical staining of the xenografts revealed that Magnolol suppressed vimentin expression and facilitated E-cadherin expression. The cytoactive detection using CCK-8 assay showed Magnolol inhibited PANC-1 and AsPC-1 concentration-dependently. Scratch healing assay and the Transwell invasion assay proved the inhibiting effects of Magnolol on cellular migration and invasion at a non-cytotoxic concentration. Western blot and rt-PCR showed that Magnolol suppressed epithelial-mesenchymal-transition by increasing the expression level of E-cadherin and decreasing those of N-cadherin and vimentin. Magnolol suppressed the TGF-β/Smad pathway by negatively regulating phosphorylation of Smad2/3. Moreover, TGF-β1 impaired the antitumor effects of Magnolol . These results demonstrated that Magnolol can inhibit proliferation, migration and invasion and by suppressing the TGF-β signal pathway and EMT. Magnolol could be a hopeful therapeutic drug for pancreatic malignancy.

摘要

厚朴酚是一种从[具体来源未给出]中提取的羟基联苯，因其抗癌潜力最近受到关注。本研究旨在探讨厚朴酚对抑制胰腺癌[细胞名称未给出]的增殖、迁移和侵袭的影响。厚朴酚在原位异种移植裸鼠模型中显示出显著的抗生长作用，对异种移植瘤的免疫组织化学染色显示厚朴酚抑制波形蛋白表达并促进E-钙黏蛋白表达。使用CCK-8法进行的细胞活性检测表明厚朴酚浓度依赖性地抑制PANC-1和AsPC-1细胞。划痕愈合试验和Transwell侵袭试验证明厚朴酚在非细胞毒性浓度下对细胞迁移和侵袭具有抑制作用。蛋白质免疫印迹法和逆转录-聚合酶链反应显示厚朴酚通过增加E-钙黏蛋白的表达水平并降低N-钙黏蛋白和波形蛋白的表达水平来抑制上皮-间质转化。厚朴酚通过负向调节Smad2/3的磷酸化来抑制TGF-β/Smad信号通路。此外，TGF-β1削弱了厚朴酚的抗肿瘤作用。这些结果表明厚朴酚可通过抑制TGF-β信号通路和上皮-间质转化来抑制[细胞名称未给出]的增殖、迁移和侵袭。厚朴酚可能是一种有希望用于治疗胰腺恶性肿瘤的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/f155e05019ad/fonc-10-597672-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/8fe7e11e2f11/fonc-10-597672-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/d3bdcaee74b1/fonc-10-597672-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/b5c1bdc68edc/fonc-10-597672-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/f155e05019ad/fonc-10-597672-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/8fe7e11e2f11/fonc-10-597672-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/c51725b40008/fonc-10-597672-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/9a9abd4e5333/fonc-10-597672-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/d22998269f1c/fonc-10-597672-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/d3bdcaee74b1/fonc-10-597672-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/b5c1bdc68edc/fonc-10-597672-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fb1/7738609/f155e05019ad/fonc-10-597672-g007.jpg

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