Dihydroartemisinin inhibits the migration of esophageal cancer cells by inducing autophagy
- Xiao Chen
- Lan-Ying He
- Shu Lai
- Yao He
Affiliations: Department of Pharmacy, Chongqing Emergency Medical Center, Chongqing University Central Hospital, Chongqing 400014, P.R. China, Department of Gastroenterology, Tumor Hospital Affiliated to Chongqing University, Chongqing 400030, P.R. China, Department of Pharmacy, Jiulongpo District People's Hospital of Chongqing, Chongqing 400050, P.R. China
- Published online on: August 6, 2020 https://doi.org/10.3892/ol.2020.11955
Copyright: © Chen
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Esophageal cancer (EC) is a complex gastrointestinal malignancy and its global incidence rate ranks 7th among all cancer types. Due to its aggressive nature and the potential for early metastasis, the survival rates of patients with EC are poor. Dihydroartemisinin (DHA) is the primary active derivative of artemisinin, and, as well as its use as an anti‑malarial, DHA has also exhibited antitumor activity in various cancer models, such as cholangiocarcinoma, head and neck carcinoma, and hepatocellular carcinoma cells. However, the molecular mechanisms underlying the antitumor effect of DHA in the treatment of EC remains poorly understood. The results of the present study demonstrated that DHA significantly inhibited the migration of TE‑1 and Eca‑109 EC cells in a dose‑dependent manner by activating autophagy. DHA treatment also significantly reversed epithelial‑mesenchymal transition (EMT) by downregulating the EMT‑associated markers, N‑cadherin and vimentin, and upregulating the expression of E‑cadherin. Mechanistically, DHA treatment decreased Akt phosphorylation and inhibited the Akt/mTOR signaling pathway, leading to the activation of autophagy. The levels of the autophagy‑associated proteins were suppressed and DHA‑mediated inhibition of migration in EC cells was reversed when an active form of Akt was overexpressed. In conclusion, the present study demonstrated the potential value of DHA in the treatment of EC, and revealed the underlying mechanism by which FDHA inhibits cellular migration.