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小豆蔻明通过抑制 NF-κB 和 mTOR 通路诱导卵巢癌细胞 G2/M 期阻滞和凋亡。

Cardamonin induces G2/M phase arrest and apoptosis through inhibition of NF-κB and mTOR pathways in ovarian cancer.

机构信息

The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou 310022, Zhejiang, China.

College of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, China.

出版信息

Aging (Albany NY). 2020 Nov 25;12(24):25730-25743. doi: 10.18632/aging.104184.

DOI:10.18632/aging.104184
PMID:33234722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7803546/
Abstract

Cardamonin, a natural chalcone, is reported to induce apoptosis and inhibit cancer cell growth. However, the mechanisms underlying the therapeutic effects of cardamonin remain to be established. Here, we have focused on cardamonin-induced apoptosis in ovarian cancer cells, both and . The effects of cardamonin on cell cycle patterns and apoptotic responses of cells were assessed in this study. Western blot was employed to determine the effects of cardamonin on expression of cell cycle- and apoptosis-related proteins. Our results indicate that cardamonin suppresses cancer cell growth by inducing G2/M phase arrest and apoptosis through targeted inhibition of NF-κB and mTOR pathways. The collective findings provide novel insights into the pathways responsible for the anticancer effects of cardamonin and support its potential utility as a clinical therapeutic agent for ovarian cancer.

摘要

小豆蔻明,一种天然的查尔酮,据报道能诱导细胞凋亡并抑制癌细胞生长。然而,小豆蔻明的治疗效果的机制尚待确定。在这里,我们集中研究了小豆蔻明诱导卵巢癌细胞凋亡,包括 和 。本研究评估了小豆蔻明对细胞周期模式和细胞凋亡反应的影响。采用蛋白质印迹法确定小豆蔻明对细胞周期和凋亡相关蛋白表达的影响。我们的结果表明,小豆蔻明通过靶向抑制 NF-κB 和 mTOR 通路,诱导 G2/M 期阻滞和细胞凋亡,从而抑制癌细胞生长。这些发现为小豆蔻明的抗癌作用的相关通路提供了新的见解,并支持其作为卵巢癌临床治疗剂的潜在用途。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/87d8e31186f5/aging-12-104184-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/f0628881ba25/aging-12-104184-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/fa59699fe8d2/aging-12-104184-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/dbc99c179dd8/aging-12-104184-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/4401b1e2f8a5/aging-12-104184-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/c002ac68cdd0/aging-12-104184-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/a94e75cf79e7/aging-12-104184-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/87d8e31186f5/aging-12-104184-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/f0628881ba25/aging-12-104184-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/fa59699fe8d2/aging-12-104184-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/dbc99c179dd8/aging-12-104184-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/4401b1e2f8a5/aging-12-104184-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/c002ac68cdd0/aging-12-104184-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/a94e75cf79e7/aging-12-104184-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61fb/7803546/87d8e31186f5/aging-12-104184-g008.jpg

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