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山奈酚通过靶向线粒体依赖性内在凋亡和 PI3K/Akt/mTOR 通路抑制雄激素非依赖性前列腺癌细胞的增殖和转移。

Isorhamnetin inhibited the proliferation and metastasis of androgen-independent prostate cancer cells by targeting the mitochondrion-dependent intrinsic apoptotic and PI3K/Akt/mTOR pathway.

机构信息

Department of Urology, The Second Affiliated Hospital of Fu Jian Medical University, Quanzhou 362000, China.

出版信息

Biosci Rep. 2020 Mar 27;40(3). doi: 10.1042/BSR20192826.

DOI:10.1042/BSR20192826
PMID:32039440
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7080645/
Abstract

The present study investigated the effects of Isorhamnetin on two types of prostate cancer cells (androgen-independent and androgen-dependent) and explored its possible mechanisms underlying such effects. Treatment with Isorhamnetin significantly inhibited cell growth and induced lactate dehydrogenase (LDH) release of androgen-independent DU145 and PC3 prostate cancer cells, but exhibited almost no toxicity effect on androgen-dependent LNCaP prostate cancer cell line or normal human prostate epithelial PrEC cells, which was achieved by the induction of apoptosis in a mitochondrion-dependent intrinsic apoptotic pathway. Furthermore, Isorhamnetin inhibited cell migration and invasion in concentration-dependent manners by enhancing mesenchymal-epithelial transition (MET) and inhibiting matrix metalloproteinase (MMP) 2 (MMP-2) and MMP-9 overexpression. In addition, Isorhamnetin also down-regulated the expression of phosphorylated PI3K (p-P13K), Akt (p-Akt), and mTOR (p-mTOR) proteins in both cancer cells, revealing Isorhamnetin to be a selective PI3K-Akt-mTOR pathway inhibitor. In summary, these findings propose that Isorhamnetin might be a novel therapeutic candidate for the treatment of androgen-independent prostate cancer.

摘要

本研究探讨了山奈酚对两种类型的前列腺癌细胞（雄激素非依赖性和雄激素依赖性）的影响，并探讨了其可能的作用机制。山奈酚处理显著抑制雄激素非依赖性 DU145 和 PC3 前列腺癌细胞的生长并诱导乳酸脱氢酶（LDH）释放，但对雄激素依赖性 LNCaP 前列腺癌细胞系或正常人类前列腺上皮 PrEC 细胞几乎没有毒性作用，这是通过诱导细胞凋亡实现的线粒体依赖性内在凋亡途径。此外，山奈酚通过增强间充质上皮转化（MET）和抑制基质金属蛋白酶（MMP）2（MMP-2）和 MMP-9 的过度表达，以浓度依赖的方式抑制细胞迁移和侵袭。此外，山奈酚还下调了两种癌细胞中磷酸化 PI3K（p-PI3K）、Akt（p-Akt）和 mTOR（p-mTOR）蛋白的表达，表明山奈酚是一种选择性的 PI3K-Akt-mTOR 通路抑制剂。总之，这些发现表明山奈酚可能是治疗雄激素非依赖性前列腺癌的一种新的治疗候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/d2a579a73371/bsr-40-bsr20192826-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/552fb141d36f/bsr-40-bsr20192826-g1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/d2a579a73371/bsr-40-bsr20192826-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/552fb141d36f/bsr-40-bsr20192826-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/17c642443001/bsr-40-bsr20192826-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/a03a3d10e35f/bsr-40-bsr20192826-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/6dfc18021031/bsr-40-bsr20192826-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/4a61329b0043/bsr-40-bsr20192826-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/4be13715b21c/bsr-40-bsr20192826-g6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea8d/7080645/d2a579a73371/bsr-40-bsr20192826-g8.jpg

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