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槲皮素通过抑制核因子-κB通路诱导人结肠癌细胞凋亡。

Quercetin induces human colon cancer cells apoptosis by inhibiting the nuclear factor-kappa B Pathway.

作者信息

Zhang Xiang-An, Zhang Shuangxi, Yin Qing, Zhang Jing

机构信息

Anorectal Disease Center, The First Affiliated Hospital, Henan College of TCM, Zhengzhou 450000, China.

Department of Hematological Malignancy, The Affiliated Hospital, Henan TCM Research Academy, Zhengzhou 450000, China.

出版信息

Pharmacogn Mag. 2015 Apr-Jun;11(42):404-9. doi: 10.4103/0973-1296.153096.

DOI:10.4103/0973-1296.153096
PMID:25829782
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4378141/
Abstract

Quercetin can inhibit the growth of cancer cells with the ability to act as chemopreventers. Its cancer-preventive effect has been attributed to various mechanisms, including the induction of cell-cycle arrest and/or apoptosis as well as the antioxidant functions. Nuclear factor kappa-B (NF-κB) is a signaling pathway that controls transcriptional activation of genes important for tight regulation of many cellular processes and is aberrantly expressed in many types of cancer. Inhibitors of NF-κB pathway have shown potential anti-tumor activities. However, it is not fully elucidated in colon cancer. In this study, we demonstrate that quercetin induces apoptosis in human colon cancer CACO-2 and SW-620 cells through inhibiting NF-κB pathway, as well as down-regulation of B-cell lymphoma 2 and up-regulation of Bax, thus providing basis for clinical application of quercetin in colon cancer cases.

摘要

槲皮素能够抑制癌细胞生长,具有化学预防剂的作用。其防癌作用归因于多种机制,包括诱导细胞周期停滞和/或凋亡以及抗氧化功能。核因子κB(NF-κB)是一种信号通路,可控制对许多细胞过程进行严格调控的重要基因的转录激活,并且在许多类型的癌症中异常表达。NF-κB通路抑制剂已显示出潜在的抗肿瘤活性。然而,在结肠癌中尚未完全阐明。在本研究中,我们证明槲皮素通过抑制NF-κB通路以及下调B细胞淋巴瘤2和上调Bax,诱导人结肠癌CACO-2和SW-620细胞凋亡,从而为槲皮素在结肠癌病例中的临床应用提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/fd14bb182594/PM-11-404-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/2c9bafa25627/PM-11-404-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/67e42cd8160d/PM-11-404-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/95ba59f4fd1a/PM-11-404-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/76d1b45ff7bd/PM-11-404-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/dace4717926f/PM-11-404-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/aa37cdc09e07/PM-11-404-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/fd14bb182594/PM-11-404-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/2c9bafa25627/PM-11-404-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/67e42cd8160d/PM-11-404-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/95ba59f4fd1a/PM-11-404-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/76d1b45ff7bd/PM-11-404-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/dace4717926f/PM-11-404-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/aa37cdc09e07/PM-11-404-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4010/4378141/fd14bb182594/PM-11-404-g007.jpg

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