Xiao-Dong Pei1,2, Zhi-Long He1, Hong-Liang Yao3, Jun-Song Xiao4, Lan Li5, Jian-Zhong Gu5, Pei-Zhao Shi5, Jin-Hua Wang5,6, Li-He Jiang7,8,9,10. 1. College of Light Industry and Food Engineering, Guangxi University, Nanning, 530004, Guangxi, People's Republic of China. 2. State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, People's Republic of China. 3. Guangdong Key Laboratory of Animal Conservation and Resource Utilization, Guangdong Public Laboratory of Wild Animal Conservation and Utilization, Institute of Zoology, Guangdong Academy of Sciences, Guangdong, 510260, People's Republic of China. 4. Beijing Higher Institution Engineering Research Center of Food Additives and Ingredients, Beijing Technology and Business University-BTBU, Beijing, 100048, People's Republic of China. 5. School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, 533000, Guangxi, People's Republic of China. 6. West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, Sichuan, People's Republic of China. 7. College of Light Industry and Food Engineering, Guangxi University, Nanning, 530004, Guangxi, People's Republic of China. jianglihe@gxu.edu.cn. 8. State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, People's Republic of China. jianglihe@gxu.edu.cn. 9. School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, 533000, Guangxi, People's Republic of China. jianglihe@gxu.edu.cn. 10. Medical College, Guangxi University, Nanning, 530004, Guangxi, People's Republic of China. jianglihe@gxu.edu.cn.
Abstract
PURPOSE: 6-Shogaol, an active phenolic compound from ginger (Zingiber officinale), can inhibit the growth of a variety of human cancer cells. Nevertheless, its underlying molecular mechanisms in cervical cancer remain unclear. In this study, we systematically examine the inhibitory effect of 6-shogaol on cervical cancer in vitro and in vivo. METHODS: Cell proliferation was assessed by CCK8 assay and colony formation assay in HeLa and SiHa cells. We analyzed cell cycle and apoptosis through flow cytometry. GFP-LC3 puncta and transmission electron microscopy were used to observe autophagic bodies. Wound-healing assay and transwell assay were used for evaluating the migration of cells. Western blot was applied to detect protein expression levels. RESULTS: 6-Shogaol could suppress cell proliferation and migration, cause cell cycle arrest in the G2/M phase in HeLa and SiHa cells. Moreover, 6-shogaol triggered the apoptosis process through the mitochondrial pathway by downregulating the expression levels of p-PI3K, p-Akt and p-mTOR. Further research indicated that the induction of apoptosis by 6-shogaol was remarkably decreased after the treatment of ROS scavenger and PI3K agonist. Additionally, 6-shogaol increased the number of LC3-positive puncta and autophagic bodies per cell in both HeLa and SiHa cells. Pretreatment of cells with Bafilomycin A1, an autophagy inhibitor, accelerated 6-shogaol mediated cell apoptosis, suggesting that induction of autophagy by 6-shogaol is suppressive to apoptosis. Furthermore, in vivo data revealed that 6-shogaol significantly inhibited tumor growth and cell proliferation in tumor tissues. CONCLUSION: These findings suggested that 6-shogaol could be developed as a functional food ingredient, which is potentially used as therapeutic agents for patients with cervical cancer.
PURPOSE:6-Shogaol, an active phenolic compound from ginger (Zingiber officinale), can inhibit the growth of a variety of humancancer cells. Nevertheless, its underlying molecular mechanisms in cervical cancer remain unclear. In this study, we systematically examine the inhibitory effect of 6-shogaol on cervical cancer in vitro and in vivo. METHODS: Cell proliferation was assessed by CCK8 assay and colony formation assay in HeLa and SiHa cells. We analyzed cell cycle and apoptosis through flow cytometry. GFP-LC3 puncta and transmission electron microscopy were used to observe autophagic bodies. Wound-healing assay and transwell assay were used for evaluating the migration of cells. Western blot was applied to detect protein expression levels. RESULTS:6-Shogaol could suppress cell proliferation and migration, cause cell cycle arrest in the G2/M phase in HeLa and SiHa cells. Moreover, 6-shogaol triggered the apoptosis process through the mitochondrial pathway by downregulating the expression levels of p-PI3K, p-Akt and p-mTOR. Further research indicated that the induction of apoptosis by 6-shogaol was remarkably decreased after the treatment of ROS scavenger and PI3K agonist. Additionally, 6-shogaol increased the number of LC3-positive puncta and autophagic bodies per cell in both HeLa and SiHa cells. Pretreatment of cells with Bafilomycin A1, an autophagy inhibitor, accelerated 6-shogaol mediated cell apoptosis, suggesting that induction of autophagy by 6-shogaol is suppressive to apoptosis. Furthermore, in vivo data revealed that 6-shogaol significantly inhibited tumor growth and cell proliferation in tumor tissues. CONCLUSION: These findings suggested that 6-shogaol could be developed as a functional food ingredient, which is potentially used as therapeutic agents for patients with cervical cancer.
Authors: Shivanand D Jolad; R Clark Lantz; Guan Jie Chen; Robert B Bates; Barbara N Timmermann Journal: Phytochemistry Date: 2005-07 Impact factor: 4.072
Authors: Shivanand D Jolad; R Clark Lantz; Aniko M Solyom; Guan Jie Chen; Robert B Bates; Barbara N Timmermann Journal: Phytochemistry Date: 2004-07 Impact factor: 4.072
Authors: Andreas C Chrysostomou; Dora C Stylianou; Anastasia Constantinidou; Leondios G Kostrikis Journal: Viruses Date: 2018-12-19 Impact factor: 5.048