ArticleBiochemistry2012
Site-specific S-nitrosylation of integrin α6 increases the extent of prostate cancer cell migration by enhancing integrin β1 association and weakening adherence to laminin-1.
Article in Biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Post-translational modifications of integrins: molecular mechanisms and pathological implications.Cellular and molecular life sciences : CMLS · 2026Review
- The evolution of S-nitrosylation detection methodology and the role of protein S-nitrosylation in various cancers.Cancer cell international · 2024Review
- S-Nitrosylation in Tumor Microenvironment.International journal of molecular sciences · 2021Review
- Roles of Integrins in Gastrointestinal Cancer Metastasis.Frontiers in molecular biosciences · 2021Review
- Computational Structural Biology ofFrontiers in oncology · 2018Review
- Accelerated migration and invasion of prostate cancer cells after a photodynamic therapy-like challenge: Role of nitric oxide.Nitric oxide : biology and chemistry · 2015Article
- Shear-induced endothelial mechanotransduction: the interplay between reactive oxygen species (ROS) and nitric oxide (NO) and the pathophysiological implications.Journal of biomedical science · 2014Review
- Molecular pathways: inflammation-associated nitric-oxide production as a cancer-supporting redox mechanism and a potential therapeutic target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The increased mortality in prostate cancer is usually the result of metastatic progression of the disease from the organ-confined location. Among the major events in this progression cascade are enhanced cell migration and loss of adhesion. Moreover, elevated levels of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) found within the tumor microenvironment are hallmarks of progression of this cancer. To understand the role of nitrosative stress in prostate cancer progression, we investigated the effects of NO and iNOS on prostate cancer cell migration and adhesion. Our results indicate that ectopic expression of iNOS in prostate cancer cells increased the extent of cell migration, which could be blocked by selective ITGα6 blocking antibody or iNOS inhibitors. Furthermore, iNOS was found to cause S-nitrosylation of ITGα6 at Cys86 in prostate cancer cells. By comparing the activities of wild-type ITGα6 and a Cys86 mutant, we showed that treatment of prostate cancer cells with NO increased the level of ITGα6 heterodimerization with ITGβ1 but not with ITGβ4. Finally, S-nitrosylation of ITGα6 weakened its binding to laminin-β1 and weakened the adhesion of prostate cancer cells to laminin-1. In conclusion, S-nitrosylation of ITGα6 increased the extent of prostate cancer cell migration, which could be a potential mechanism of NO- and iNOS-induced enhancement of prostate cancer metastasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.