Triptolide suppresses IL-1β-induced expression of interleukin-8 by inhibiting ROS-Mediated ERK, AP-1, and NF-κB molecules in human gastric cancer AGS cells

Triptolide, the major component of Chinese herbal medicine Tripterygium wilfordii Hook F, possesses potent anticancer and anti-inflammatory effects. IL-8, a proinflammatory cytokine, is associated with cancer cell proliferation and angiogenesis. Here, we found that Triptolide has an inhibitory effec...

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Main Authors: Shinan Li, Dhiraj Kumar Sah, Archana Arjunan, Mohamed Yazeer Ameer, Bora Lee, Young-Do Jung
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-01-01
Series:Frontiers in Oncology
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Online Access:https://www.frontiersin.org/articles/10.3389/fonc.2024.1498213/full
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author Shinan Li
Shinan Li
Dhiraj Kumar Sah
Archana Arjunan
Mohamed Yazeer Ameer
Bora Lee
Young-Do Jung
author_facet Shinan Li
Shinan Li
Dhiraj Kumar Sah
Archana Arjunan
Mohamed Yazeer Ameer
Bora Lee
Young-Do Jung
author_sort Shinan Li
collection DOAJ
description Triptolide, the major component of Chinese herbal medicine Tripterygium wilfordii Hook F, possesses potent anticancer and anti-inflammatory effects. IL-8, a proinflammatory cytokine, is associated with cancer cell proliferation and angiogenesis. Here, we found that Triptolide has an inhibitory effect on IL-1β-induced IL-8 expression in human gastric cancer cells, via the suppression of reactive oxygen species (ROS) production, AP-1, and NF-κB activation, which in turn affects human endothelial cell angiogenetic activity in tumor microenvironments. Human gastric AGS cells were treated with IL-1β (10 ng/mL) and Triptolide (0–20 nM), and the ROS generation, ERK, AP-1, and NF-κB signaling were all investigated. These results demonstrate that Triptolide inhibits the IL-1β-induced IL-8 expression in gastric cancer cells by inhibiting ROS production and angiogenesis, via the dose-dependent attenuation of ERK, AP-1, and NF-κB activation. In this study, we showed that Triptolid inhibits ROS/ERK-mediated AP-1 and ROS-mediated NF-κB axes potentially leading to an improved treatment outcome for gastric cancer and its associated tumor microenvironment.
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issn 2234-943X
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spelling doaj-art-cf6ebcb125d7485cb81830d911c74f272025-01-30T05:10:18ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2025-01-011410.3389/fonc.2024.14982131498213Triptolide suppresses IL-1β-induced expression of interleukin-8 by inhibiting ROS-Mediated ERK, AP-1, and NF-κB molecules in human gastric cancer AGS cellsShinan Li0Shinan Li1Dhiraj Kumar Sah2Archana Arjunan3Mohamed Yazeer Ameer4Bora Lee5Young-Do Jung6Department of Biochemistry and Molecular Biology, School of Basic Medicine, Shanxi Medical University, Taiyuan, ChinaDepartment of Biochemistry, Chonnam National University Medical School, Hwasun, Republic of KoreaDepartment of Biochemistry, Chonnam National University Medical School, Hwasun, Republic of KoreaDepartment of Biochemistry, Chonnam National University Medical School, Hwasun, Republic of KoreaDepartment of Biochemistry, Chonnam National University Medical School, Hwasun, Republic of KoreaDepartment of Biochemistry, Chonnam National University Medical School, Hwasun, Republic of KoreaDepartment of Biochemistry, Chonnam National University Medical School, Hwasun, Republic of KoreaTriptolide, the major component of Chinese herbal medicine Tripterygium wilfordii Hook F, possesses potent anticancer and anti-inflammatory effects. IL-8, a proinflammatory cytokine, is associated with cancer cell proliferation and angiogenesis. Here, we found that Triptolide has an inhibitory effect on IL-1β-induced IL-8 expression in human gastric cancer cells, via the suppression of reactive oxygen species (ROS) production, AP-1, and NF-κB activation, which in turn affects human endothelial cell angiogenetic activity in tumor microenvironments. Human gastric AGS cells were treated with IL-1β (10 ng/mL) and Triptolide (0–20 nM), and the ROS generation, ERK, AP-1, and NF-κB signaling were all investigated. These results demonstrate that Triptolide inhibits the IL-1β-induced IL-8 expression in gastric cancer cells by inhibiting ROS production and angiogenesis, via the dose-dependent attenuation of ERK, AP-1, and NF-κB activation. In this study, we showed that Triptolid inhibits ROS/ERK-mediated AP-1 and ROS-mediated NF-κB axes potentially leading to an improved treatment outcome for gastric cancer and its associated tumor microenvironment.https://www.frontiersin.org/articles/10.3389/fonc.2024.1498213/fullangiogenesisERK1/2gastric cancerInterleukin-1ßreactive oxygen speciestriptolide
spellingShingle Shinan Li
Shinan Li
Dhiraj Kumar Sah
Archana Arjunan
Mohamed Yazeer Ameer
Bora Lee
Young-Do Jung
Triptolide suppresses IL-1β-induced expression of interleukin-8 by inhibiting ROS-Mediated ERK, AP-1, and NF-κB molecules in human gastric cancer AGS cells
Frontiers in Oncology
angiogenesis
ERK1/2
gastric cancer
Interleukin-1ß
reactive oxygen species
triptolide
title Triptolide suppresses IL-1β-induced expression of interleukin-8 by inhibiting ROS-Mediated ERK, AP-1, and NF-κB molecules in human gastric cancer AGS cells
title_full Triptolide suppresses IL-1β-induced expression of interleukin-8 by inhibiting ROS-Mediated ERK, AP-1, and NF-κB molecules in human gastric cancer AGS cells
title_fullStr Triptolide suppresses IL-1β-induced expression of interleukin-8 by inhibiting ROS-Mediated ERK, AP-1, and NF-κB molecules in human gastric cancer AGS cells
title_full_unstemmed Triptolide suppresses IL-1β-induced expression of interleukin-8 by inhibiting ROS-Mediated ERK, AP-1, and NF-κB molecules in human gastric cancer AGS cells
title_short Triptolide suppresses IL-1β-induced expression of interleukin-8 by inhibiting ROS-Mediated ERK, AP-1, and NF-κB molecules in human gastric cancer AGS cells
title_sort triptolide suppresses il 1β induced expression of interleukin 8 by inhibiting ros mediated erk ap 1 and nf κb molecules in human gastric cancer ags cells
topic angiogenesis
ERK1/2
gastric cancer
Interleukin-1ß
reactive oxygen species
triptolide
url https://www.frontiersin.org/articles/10.3389/fonc.2024.1498213/full
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