Xue Hu1,2, Jingjing Ma1, Vikash Vikash1, Jiao Li1, Dandan Wu1, Ya Liu1, Jixiang Zhang1, Weiguo Dong3. 1. Department of Gastroenterology, Renmin Hospital of Wuhan University, No. 99 Zhang Zhi-dong Road, Wuhan, 430060, Hubei Province, People's Republic of China. 2. Key Laboratory of Hubei Province for Digestive System Disease, Wuhan, Hubei Province, People's Republic of China. 3. Department of Gastroenterology, Renmin Hospital of Wuhan University, No. 99 Zhang Zhi-dong Road, Wuhan, 430060, Hubei Province, People's Republic of China. dwg@whu.edu.cn.
Abstract
BACKGROUND: Thymoquinone (TQ) is the major constituent of Nigella sativa seed and has shown biological activity in various human carcinomas. However, few studies have reported its effect on esophageal carcinoma (EC). AIMS: To explore the chemosensitive effect and mechanism of TQ in augmentation of cisplatin (DDP)-induced apoptosis of EC, both in vitro and in vivo. METHODS: The viability and apoptosis of esophageal carcinoma cells were detected by the Cell Counting Kit-8 assay, flow cytometry, and Hoechst 33258 staining. The expression levels of JAK2, p-JAK2, STAT3, p-STAT3, Bax, Bcl-2, Cyclin D1, Survivin, and caspase-3, 7, 9 were evaluated by western blot analysis. The histological changes were examined by TUNEL technique and immunohistochemical analysis. RESULTS: TQ enhanced the proapoptotic effect of DDP in human esophageal carcinoma cell line Eca-109, while blocking the activation of JAK2/STAT3 signaling pathway. The apoptosis of esophageal carcinoma cells was induced via blocking the activation of JAK2/STAT3 by using a molecular inhibitor (WP1066). Consistent with the in vivo and in vitro results, TQ increased cellular apoptosis and enriched the chemosensitivity of DDP. CONCLUSIONS: TQ along with DDP may regulate the progression of EC and has potential to be a chemotherapeutic agent in EC.
BACKGROUND:Thymoquinone (TQ) is the major constituent of Nigella sativa seed and has shown biological activity in various humancarcinomas. However, few studies have reported its effect on esophageal carcinoma (EC). AIMS: To explore the chemosensitive effect and mechanism of TQ in augmentation of cisplatin (DDP)-induced apoptosis of EC, both in vitro and in vivo. METHODS: The viability and apoptosis of esophageal carcinoma cells were detected by the Cell Counting Kit-8 assay, flow cytometry, and Hoechst 33258 staining. The expression levels of JAK2, p-JAK2, STAT3, p-STAT3, Bax, Bcl-2, Cyclin D1, Survivin, and caspase-3, 7, 9 were evaluated by western blot analysis. The histological changes were examined by TUNEL technique and immunohistochemical analysis. RESULTS:TQ enhanced the proapoptotic effect of DDP in humanesophageal carcinoma cell line Eca-109, while blocking the activation of JAK2/STAT3 signaling pathway. The apoptosis of esophageal carcinoma cells was induced via blocking the activation of JAK2/STAT3 by using a molecular inhibitor (WP1066). Consistent with the in vivo and in vitro results, TQ increased cellular apoptosis and enriched the chemosensitivity of DDP. CONCLUSIONS:TQ along with DDP may regulate the progression of EC and has potential to be a chemotherapeutic agent in EC.
Authors: Benjamin Barré; Arnaud Vigneron; Neil Perkins; Igor B Roninson; Erick Gamelin; Olivier Coqueret Journal: Trends Mol Med Date: 2006-11-21 Impact factor: 11.951
Authors: Jacques Ferlay; Isabelle Soerjomataram; Rajesh Dikshit; Sultan Eser; Colin Mathers; Marise Rebelo; Donald Maxwell Parkin; David Forman; Freddie Bray Journal: Int J Cancer Date: 2014-10-09 Impact factor: 7.396
Authors: Dan-Dan Xu; Men Ding; Pan Tong; Yan-Yun Chong; Wei-Yu Gu; Yang Li; Xin-Jiang Fang; Ning Li Journal: Oncol Rep Date: 2020-07-07 Impact factor: 3.906