Journal
EUROPEAN JOURNAL OF NUTRITION
Volume 60, Issue 5, Pages 2781-2793Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00394-020-02440-9
Keywords
6-Shogaol; Apoptosis; Cell migration; Autophagy; PI3K/Akt/mTOR pathway
Categories
Funding
- 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 [GTZK201810]
- Key laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Ministry of Education [GKE2018-KF01]
- Guangdong Academic of Sciences Special Project of Science and Technology Development [2016GDASRC-0104]
- Guangdong Key Laboratory of Animal Conservation and Resource Utilization [GIABR-KF201901]
- Beijing Engineering and Technology Research Center of Food Additives, Beijing Technology & Business University (BTBU)
- Open Project of Hubei Key Laboratory of Wudang Local Chinese Medicine Research (Hubei University of Medicine) [WDCM2019012]
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6-Shogaol, an active compound from ginger, inhibits cell proliferation and migration in cervical cancer cells, induces cell cycle arrest at G2/M phase, and triggers apoptosis through the mitochondrial pathway by downregulating expression levels of related proteins.
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.
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