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• W2765282783 abstract "// Su Jin Kang 1, 2, * , Young Joon Lee 1, 2, * , Sung Gu Kang 3 , Soyoung Cho 4, 5 , Wonsuck Yoon 6 , Ji Hong Lim 7 , Sang-Hyun Min 8 , Tae Ho Lee 9 and Byeong Mo Kim 5 1 The Medical Research Center for Globalization of Herbal Medicine, Daegu Haany University, Gyeongsan, Gyeongsangbuk-Do 38610, Republic of Korea 2 Department of Preventive Medicine, College of Korean Medicine, Daegu Haany University, Gyeongsan, Gyeongsangbuk-Do 38610, Republic of Korea 3 Department of Urology, Korea University College of Medicine, Seongbuk-gu, Seoul 02841, Republic of Korea 4 Department of Science for Aging, Yonsei University, Seodaemun-gu, Seoul 03722, Republic of Korea 5 Severance Integrative Research Institute for Cerebral & Cardiovascular Diseases (SIRIC), Yonsei University College of Medicine, Seodaemun-gu, Seoul 03722, Republic of Korea 6 Allergy Immunology Center, Korea University College of Medicine, Seongbuk-gu, Seoul 02841, Republic of Korea 7 Department of Biomedical Chemistry, Konkuk University, Chungju, Chungbuk 27478, Republic of Korea 8 New Drug Development Center, DGMIF, Dong-gu, Daegu 41061, Republic of Korea 9 Division of Gerontology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA * These authors have contributed equally to this work Correspondence to: Byeong Mo Kim, email: bkim2@yuhs.ac Keywords: saikosaponin a (SSa); human colon carcinoma (HCC); endoplasmic reticulum (ER) stress; caspase-4; DNA damage Received: March 29, 2017     Accepted: September 30, 2017     Published: November 01, 2017 ABSTRACT Saikosaponin a (SSa), a bioactive phytochemical from Bupleurum , triggers sequential caspase-2 and caspase-8 activation, and thereby induces caspase-mediated apoptosis in human colon carcinoma (HCC) cells. However, the upstream mechanism of caspase-2 activation remains unknown. Therefore, we investigated the signaling mechanisms underlying SSa-induced caspase activation and apoptosis in HCC cells. SSa treatment triggered marked antitumor effects, especially in HCC cells, in a cell culture model and a mouse xenograft model. SSa also induced the activation of several endoplasmic reticulum (ER) stress signals. Specifically, caspase-4, a critical regulator of ER stress-induced apoptosis, was activated significantly after SSa treatment. Mechanistically, selective inhibition of caspase-4 suppressed SSa-induced apoptosis, colony inhibition, and the activation of caspase-3, -8, and -2, but not vice versa . Consistent with the important role of caspase-2 in the DNA damage response, SSa induced DNA damage, as evidenced by a cytokinesis-block micronucleus assay, single-cell gel electrophoresis, and an increase in the levels of γ-H2AX, a DNA damage marker. Moreover, inhibition of caspase-4 activation inhibited SSa-induced histone H2AX phosphorylation. Taken together, these results suggest that caspase-4 is an upstream regulator of SSa-induced DNA damage and caspase activation in HCC cells. Given that SSa-induced apoptosis appeared to be specific to certain cell types including HCC cells, SSa may be a promising cancer therapy agent in certain types of cancer." @default.
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• W2765282783 date "2017-11-01" @default.
• W2765282783 modified "2023-10-17" @default.
• W2765282783 title "Caspase-4 is essential for saikosaponin a-induced apoptosis acting upstream of caspase-2 and γ-H2AX in colon cancer cells" @default.
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• W2765282783 doi "https://doi.org/10.18632/oncotarget.22247" @default.
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