Abstract | INTRODUCTION: A catalytic subunit of NADPH oxidase 1 (Nox1) is implicated to be involved in neoplastic progression in human epithelial cancers. We had previously demonstrated that Nox1 overexpression of immortalized epithelial cells was able to induce the generation of progenitor cells that expressed fetal-type cytokeratins 8 and 18. PURPOSE: We aimed to investigate the direct effects and underlying mechanisms of Nox1 on expression of cytokeratin 18 (CK18). METHODS: Immortalized human epithelial GM16 cells with low CK18 were used in Nox1 overexpression experiments. NuB2 cells with high CK18 were used in Nox1 knockdown experiments. Protein expression of CK18, phosphorylated and ubiquitinated CK18 were analyzed by Western blot. RESULTS: CONCLUSION: We demonstrated that Nox1 was able to induce CK18 stabilization by inhibiting CK18 protein degradation in a phosphorylation-dependent manner. CK18 accumulation induced by Nox1 is consistent with the persistence of fetal-type CK18 protein in many epithelial carcinomas.
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Authors | Apsorn Sattayakhom, Wanida Ittiwat, Wolfgang Stremmel, Walee Chamulitrat |
Journal | Journal of cancer research and clinical oncology
(J Cancer Res Clin Oncol)
Vol. 137
Issue 11
Pg. 1669-78
(Nov 2011)
ISSN: 1432-1335 [Electronic] Germany |
PMID | 21877197
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Keratin-18
- RNA, Messenger
- Reactive Oxygen Species
- NADH, NADPH Oxidoreductases
- NADPH Oxidase 1
- NADPH Oxidases
- NOX1 protein, human
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Topics |
- Cell Transformation, Neoplastic
(metabolism)
- Epithelial Cells
(metabolism)
- Gene Expression Regulation, Enzymologic
- Gene Expression Regulation, Neoplastic
- Humans
- Keratin-18
(genetics, metabolism)
- NADH, NADPH Oxidoreductases
(genetics, metabolism)
- NADPH Oxidase 1
- NADPH Oxidases
(metabolism)
- Oxidation-Reduction
- Phosphorylation
- RNA, Messenger
(metabolism)
- Reactive Oxygen Species
(metabolism)
- Ubiquitination
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