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Action of the natural compound gomisin a on Ca2+ movement in human prostate cancer cells
Lyh-Jyh Hao1, Rong-An Lin2, Li-Chai Chen3, Jue-Long Wang4, I-Shu Chen5, Chun-Chi Kuo6, Chiang-Ting Chou7, Jau-Min Chien8, Chung-Ren Jan9
1 Department of Endocrinology and Metabolism, Kaohsiung Veteran General Hospital, Tainan Branch; Department of Nursing, Chung Hwa University of Medical Technology, Tainan, Taiwan
2 Department of Pharmacy, Kaohsiung Veterans General Hospital, Tainan Branch; Department of Pharmaceutical Science and Technology, Chung Hwa University of Medical Technology, Tainan, Taiwan
3 Department of Pharmacy, Tajen University, Ping Tung, Taiwan
4 Department of Rehabilitation, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
5 Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
6 Department of Nursing, Tzu Hui Institute of Technology, Pingtung, Taiwan
7 Department of Nursing, Division of Basic Medical Sciences, Chang Gung University of Science and Technology, Puzi City, Chiayi County, Taiwan
8 Department of Pediatrics, Pingtung Christian Hospital, Pingtung, Taiwan
9 Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Correspondence Address:
Prof. Chung-Ren Jan
No. 386, Dazhong 1st Road, Zuoying Dist, Kaohsiung City 81362
Taiwan
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/cjp.cjp_6_22
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Gomisin A is a dietary lignan compound isolated from the fruit of Schisandra chinensis and has many pharmacological properties, including hepato-protective, anti-diabetic, and anti-oxidative activities. However, the benefit of gomisin A is still not well understood. The action of gomisin A is diverse. However, the effect of gomisin A on Ca2+ signaling in prostate cancer cells is unknown. Ca2+ is a pivotal second envoy that triggers and regulates cellular processes such as apoptosis, fertilization, energy transduction, secretion, and protein activation. The goal of this study was to explore the action of gomisin A on [Ca2+]i and cytotoxicity in PC3 prostate cancer cells. Gomisin A at 100–200 μM provoked [Ca2+]i raises. 20% of the response was reduced by removing external Ca2+. The Ca2+ influx provoked by gomisin A was suppressed by 20% by store-caused Ca2+ entry suppressors: econazole, SKF96365, nifedipine; also by phorbol 12-myristate 13 acetate and GF109203X. Without external Ca2+, gomisin A-caused [Ca2+]i raises were abolished by thapsigargin. In contrast, gomisin A suppressed the [Ca2+]i raises caused by thapsigargin. U73122 fell short to change gomisin A-caused [Ca2+]i responses. Gomisin A (20–100 μM) elicited cytotoxicity in a dose-associated fashion. Blockade of [Ca2+] elevations with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl failed to inhibit cytotoxicity of gomisin A. Collectively, gomisin A evoked [Ca2+]i raises and provoked cytotoxicity in a Ca2+-dissociated fashion in prostate cancer cells.
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