Changes in mitochondrial function during EMT induced by TGFβ-1 in pancreatic cancer

Guo,Qingqu

doi:10.3892/ol.2017.5613

Changes in mitochondrial function during EMT induced by TGFβ-1 in pancreatic cancer

Authors:
- Qingqu Guo
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Affiliations: Department of Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China
Published online on: January 18, 2017 https://doi.org/10.3892/ol.2017.5613
Pages: 1575-1580
Copyright: © Guo . This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Mitochondrial dysfunction is linked to cancer. Differences in the number, morphology and function of mitochondria have been observed between normal cells and cancer cells. However, changes in mitochondrial function during epithelial-mesenchymal transition (EMT) in pancreatic cancer are less known. In the present study, the cultured human pancreatic cancer cell line Panc‑1 was treated with transforming growth factor (TGF)β‑1. Mitochondrial functions following TGFβ‑1 exposure in pancreatic cancer were investigated. It was noticed that TGFβ‑1 treatment induces morphologic changes and a shift from epithelial to mesenchymal phenotype in pancreatic cancer. Furthermore, increased mitochondrial mass was detected in pancreatic cancer following TGFβ‑1 treatment. Besides, the production of reactive oxygen species in TGFβ-1-treated pancreatic cancer cells significantly increased compared with the control cells. Our results indicate that the phenomenon of EMT in pancreatic cancer has an association with mitochondrial dysfunction. Mitochondrial dysfunction may be a cause of EMT in pancreatic cancer, which leads to heterogeneity in pancreatic cancer, and may be a potential therapeutic target in the future.

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