Iron chelator-induced apoptosis via the ER stress pathway in gastric cancer cells
- Authors
- Kim, Jung Lim; Lee, Dae-Hee; Na, Yoo Jin; Kim, Bo Ram; Jeong, Yoon A.; Lee, Sun Il; Kang, Sanghee; Joung, Sung Yup; Lee, Suk-Young; Oh, Sang Cheul; Min, Byung Wook
- Issue Date
- Jul-2016
- Publisher
- SAGE PUBLICATIONS LTD
- Keywords
- Iron chelator; Gastric cancer; ER stress; JNK
- Citation
- TUMOR BIOLOGY, v.37, no.7, pp 9709 - 9719
- Pages
- 11
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- TUMOR BIOLOGY
- Volume
- 37
- Number
- 7
- Start Page
- 9709
- End Page
- 9719
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/6260
- DOI
- 10.1007/s13277-016-4878-4
- ISSN
- 1010-4283
1423-0380
- 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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- Appears in
Collections - 3. Graduate School > Graduate School > 1. Journal Articles
- 4. Research institute > Institute of Convergence New Drug Development > 1. Journal Articles
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