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白茅提取物对前列腺癌发生及去势抵抗性前列腺癌的抑制作用及分子机制

Suppressive Effect and Molecular Mechanism of Thunb. Extract against Prostate Carcinogenesis and Castration-Resistant Prostate Cancer.

作者信息

Subhawa Subhawat, Naiki-Ito Aya, Kato Hiroyuki, Naiki Taku, Komura Masayuki, Nagano-Matsuo Aya, Yeewa Ranchana, Inaguma Shingo, Chewonarin Teera, Banjerdpongchai Ratana, Takahashi Satoru

机构信息

Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, 1-Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan.

Department of Biochemistry, Faculty of Medicine, Chiang Mai University, 110 Intravaroros Rd., Sripoom, Muang, Chiang Mai 50200, Thailand.

出版信息

Cancers (Basel). 2021 Jul 7;13(14):3403. doi: 10.3390/cancers13143403.

DOI:10.3390/cancers13143403
PMID:34298624
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8306559/
Abstract

Thunb. (HCT) is a well-known Asian medicinal plant with biological activities used in the treatment of many diseases including cancer. This study investigated the effects of HCT extract and its ethyl acetate fraction (EA) on prostate carcinogenesis and castration-resistant prostate cancer (CRPC). HCT and EA induced apoptosis in androgen-sensitive prostate cancer cells (LNCaP) and CRPC cells (PCai1) through activation of caspases, down-regulation of androgen receptor, and inactivation of AKT/ERK/MAPK signaling. Rutin was found to be a major component in HCT (44.00 ± 5.61 mg/g) and EA (81.34 ± 5.21 mg/g) in a previous study. Rutin had similar effects to HCT/EA on LNCaP cells and was considered to be one of the active compounds. Moreover, HCT/EA inhibited cell migration and epithelial-mesenchymal transition phenotypes via STAT3/Snail/Twist pathways in LNCaP cells. The consumption of 1% HCT-mixed diet significantly decreased the incidence of adenocarcinoma in the lateral prostate lobe of the Transgenic rat for adenocarcinoma of prostate model. Similarly, tumor growth of PCai1 xenografts was significantly suppressed by 1% HCT treatment. HCT also induced caspase-dependent apoptosis via AKT inactivation in both in vivo models. Together, the results of in vitro and in vivo studies indicate that HCT has inhibitory effects against prostate carcinogenesis and CRPC. This plant therefore should receive more attention as a source for the future development of non-toxic chemopreventive agents against various cancers.

摘要

刺蒺藜（HCT）是一种著名的亚洲药用植物，具有生物活性，可用于治疗包括癌症在内的多种疾病。本研究调查了HCT提取物及其乙酸乙酯馏分（EA）对前列腺癌发生和去势抵抗性前列腺癌（CRPC）的影响。HCT和EA通过激活半胱天冬酶、下调雄激素受体以及使AKT/ERK/MAPK信号失活，诱导雄激素敏感的前列腺癌细胞（LNCaP）和CRPC细胞（PCai1）凋亡。在先前的一项研究中发现，芦丁是HCT（44.00±5.61毫克/克）和EA（81.34±5.21毫克/克）中的主要成分。芦丁对LNCaP细胞具有与HCT/EA相似的作用，被认为是活性化合物之一。此外，HCT/EA通过LNCaP细胞中的STAT3/蜗牛蛋白/ Twist途径抑制细胞迁移和上皮-间质转化表型。食用1% HCT混合饲料显著降低了前列腺癌转基因大鼠模型侧叶前列腺腺癌的发生率。同样，1% HCT处理显著抑制了PCai1异种移植瘤的生长。在两种体内模型中，HCT还通过AKT失活诱导半胱天冬酶依赖性凋亡。总之，体外和体内研究结果表明，HCT对前列腺癌发生和CRPC具有抑制作用。因此，这种植物作为未来开发针对各种癌症的无毒化学预防剂的来源，应受到更多关注。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/964db4d3084d/cancers-13-03403-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/35c767f46027/cancers-13-03403-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/96de21865450/cancers-13-03403-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/e093c8e99bdd/cancers-13-03403-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/d029b0c561ba/cancers-13-03403-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/86c8808cf185/cancers-13-03403-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/8a1bc2f58eec/cancers-13-03403-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/2c7b6fa541cf/cancers-13-03403-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/c694972314a8/cancers-13-03403-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/d82befb8f115/cancers-13-03403-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/964db4d3084d/cancers-13-03403-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/35c767f46027/cancers-13-03403-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/96de21865450/cancers-13-03403-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/e093c8e99bdd/cancers-13-03403-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/d029b0c561ba/cancers-13-03403-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/86c8808cf185/cancers-13-03403-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/8a1bc2f58eec/cancers-13-03403-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/2c7b6fa541cf/cancers-13-03403-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/c694972314a8/cancers-13-03403-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/d82befb8f115/cancers-13-03403-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee19/8306559/964db4d3084d/cancers-13-03403-g010.jpg

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