Research Paper Volume 12, Issue 11 pp 11116—11138

Deoxyelephantopin induces apoptosis via oxidative stress and enhances gemcitabine sensitivity in vitro and in vivo through targeting the NF-κB signaling pathway in pancreatic cancer

Daolin Ji1,2, , Xiangyu Zhong1, , Peng Huang1,2, , Pengcheng Kang1, , Kaiming Leng3, , Wangyang Zheng1,2, , Zhidong Wang1, , Yi Xu1,2, , Yunfu Cui1, ,

  • 1 Department of Hepatopancreatobiliary Surgery, The Second Affiliated Hospital, Harbin Medical University, Harbin, China
  • 2 The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Ministry of Education, Harbin, China
  • 3 Department of Hepatobiliary Surgery, Qingdao Municipal Hospital, Qingdao, China

Received: October 7, 2019       Accepted: March 29, 2020       Published: June 11, 2020
How to Cite

Copyright © 2020 Ji et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Pancreatic cancer is a highly invasive malignant tumor of the digestive system with an unfavorable prognosis worldwide. This trait is thought to be largely attributed to chemoresistance. Chemotherapy is the only hope for patients with advanced pancreatic cancer. Therefore, seeking new effective chemotherapy drugs has become an urgent need. The purpose of our study was to explore whether deoxyelephantopin (DET), a sesquiterpene lactone, has a potential antitumor effect in pancreatic cancer. Additionally, the antitumor effects of DET alone or in combination with gemcitabine (GEM) and the potential mechanism of this combination were revealed. In vitro experiments showed that DET suppressed the proliferation, invasion and metastasis of pancreatic cancer cells, induced cell apoptosis via oxidative stress, and enhanced GEM sensitivity by inhibiting the NF-κB signaling pathway. Beyond that, in vivo experiments showed that DET not only inhibited pancreatic tumor growth and metastasis but also amplified the antitumor capacity of GEM, which was related to the downregulation of NF-κB and its downstream gene products. In summary, it is possible that DET could be developed as a single agent or combined with conventional chemotherapy drugs to improve the treatment of pancreatic cancer.


DET: deoxyelephantopin; GEM: gemcitabine; ROS: reactive oxygen species; MMP: mitochondrial membrane potential; DCFH-DA: 2’, 7’-dichlorofluorescein-diacetate; NAC: N-acetylcysteine; CCK-8: cell counting kit-8; AO/EB: acridine orange/ethidium bromide; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; IκB: nuclear factor-kappa B inhibitor; IKK: IκB kinase inhibitor; TNF-α: tumour necrosis factor alpha; EMT: epithelial-mesenchymal transition; IHC: immunohistochemistry; H&E: hemotoxylin and eosin staining.