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Erschienen in: Tumor Biology 7/2016

23.01.2016 | Original Article

Iron chelator-induced apoptosis via the ER stress pathway in gastric cancer cells

verfasst von: Jung Lim Kim, Dae-Hee Lee, Yoo Jin Na, Bo Ram Kim, Yoon A. Jeong, Sun Il Lee, Sanghee Kang, Sung Yup Joung, Suk-Young Lee, Sang Cheul Oh, Byung Wook Min

Erschienen in: Tumor Biology | Ausgabe 7/2016

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Abstract

Many reports have shown the anticancer effects of iron deficient on cancer cells, but the effects of iron-chelators on gastric cancer have not been clearly elucidated. Recently, we reported that iron chelators induced an antiproliferative effect in human malignant lymphoma and myeloid leukemia cells. In the present study, we investigated the antitumor activity of these two iron-chelating agents, deferoxamine (DFO) and deferasirox (DFX), with gastric cancer cell lines, and their apoptosis-inducing effects as the potential mechanism. We found that iron chelators displayed significant antiproliferative activity in human gastric cancer cell lines, which may be attributed to their induction of G1 phase arrest and apoptosis. We also found that iron chelators induced reactive oxygen species (ROS) production, resulting in the activation of both c-Jun N-terminal kinase (JNK) and endoplasmic reticulum (ER) stress apoptotic pathways in gastric cancer cells. Taken together, our data suggest that iron chelators induced apoptosis in gastric cancer, involving ROS formation ER stress and JNK activation.
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Metadaten
Titel
Iron chelator-induced apoptosis via the ER stress pathway in gastric cancer cells
verfasst von
Jung Lim Kim
Dae-Hee Lee
Yoo Jin Na
Bo Ram Kim
Yoon A. Jeong
Sun Il Lee
Sanghee Kang
Sung Yup Joung
Suk-Young Lee
Sang Cheul Oh
Byung Wook Min
Publikationsdatum
23.01.2016
Verlag
Springer Netherlands
Erschienen in
Tumor Biology / Ausgabe 7/2016
Print ISSN: 1010-4283
Elektronische ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-016-4878-4

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