GPI-80 Augments NF-κB Activation in Tumor Cells

Recent studies have discovered a relationship between glycosylphosphatidylinositol (GPI)-anchored protein 80 (GPI-80)/VNN2 (80 kDa GPI-anchored protein) and malignant tumors. GPI-80 is known to regulate neutrophil adhesion; however, the action of GPI-80 on tumors is still obscure. In this study, alt...

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Autores principales: Yuji Takeda, Yuta Kurota, Tomoyuki Kato, Hiromi Ito, Akemi Araki, Hidetoshi Nara, Shinichi Saitoh, Nobuyuki Tanaka, Norihiko Tsuchiya, Hironobu Asao
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/a5810e6cad8b464db0454c85916ff062
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spelling oai:doaj.org-article:a5810e6cad8b464db0454c85916ff0622021-11-11T17:25:45ZGPI-80 Augments NF-κB Activation in Tumor Cells10.3390/ijms2221120271422-00671661-6596https://doaj.org/article/a5810e6cad8b464db0454c85916ff0622021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/12027https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Recent studies have discovered a relationship between glycosylphosphatidylinositol (GPI)-anchored protein 80 (GPI-80)/VNN2 (80 kDa GPI-anchored protein) and malignant tumors. GPI-80 is known to regulate neutrophil adhesion; however, the action of GPI-80 on tumors is still obscure. In this study, although the expression of GPI-80 mRNA was detectable in several tumor cell lines, the levels of GPI-80 protein were significantly lower than that in neutrophils. To clarify the function of GPI-80 in tumor cells, GPI-80-expressing cells and GPI-80/VNN2 gene-deleted cells were established using PC3 prostate cancer cells. In GPI-80-expressing cells, GPI-80 was mainly detected in vesicles. Furthermore, soluble GPI-80 in the conditioned medium was associated with the exosome marker CD63 and was also detected in the plasma obtained from prostate cancer patients. Unexpectedly, cell adhesion and migration of GPI-80-expressing PC3 cells were not modulated by anti-GPI-80 antibody treatment. However, similar to the GPI-80 family molecule, VNN1, the pantetheinase activity and oxidative state were augmented in GPI-80-expressing cells. GPI-80-expressing cells facilitated non-adhesive proliferation, slow cell proliferation, NF-κB activation and IL-1β production. These phenomena are known to be induced by physiological elevation of the oxidative state. Thus, these observations indicated that GPI-80 affects various tumor responses related to oxidation.Yuji TakedaYuta KurotaTomoyuki KatoHiromi ItoAkemi ArakiHidetoshi NaraShinichi SaitohNobuyuki TanakaNorihiko TsuchiyaHironobu AsaoMDPI AGarticleIL-1βNF-κBoxidative stresspantetheinaseprostate cancer cellsBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12027, p 12027 (2021)
institution DOAJ
collection DOAJ
language EN
topic IL-1β
NF-κB
oxidative stress
pantetheinase
prostate cancer cells
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle IL-1β
NF-κB
oxidative stress
pantetheinase
prostate cancer cells
Biology (General)
QH301-705.5
Chemistry
QD1-999
Yuji Takeda
Yuta Kurota
Tomoyuki Kato
Hiromi Ito
Akemi Araki
Hidetoshi Nara
Shinichi Saitoh
Nobuyuki Tanaka
Norihiko Tsuchiya
Hironobu Asao
GPI-80 Augments NF-κB Activation in Tumor Cells
description Recent studies have discovered a relationship between glycosylphosphatidylinositol (GPI)-anchored protein 80 (GPI-80)/VNN2 (80 kDa GPI-anchored protein) and malignant tumors. GPI-80 is known to regulate neutrophil adhesion; however, the action of GPI-80 on tumors is still obscure. In this study, although the expression of GPI-80 mRNA was detectable in several tumor cell lines, the levels of GPI-80 protein were significantly lower than that in neutrophils. To clarify the function of GPI-80 in tumor cells, GPI-80-expressing cells and GPI-80/VNN2 gene-deleted cells were established using PC3 prostate cancer cells. In GPI-80-expressing cells, GPI-80 was mainly detected in vesicles. Furthermore, soluble GPI-80 in the conditioned medium was associated with the exosome marker CD63 and was also detected in the plasma obtained from prostate cancer patients. Unexpectedly, cell adhesion and migration of GPI-80-expressing PC3 cells were not modulated by anti-GPI-80 antibody treatment. However, similar to the GPI-80 family molecule, VNN1, the pantetheinase activity and oxidative state were augmented in GPI-80-expressing cells. GPI-80-expressing cells facilitated non-adhesive proliferation, slow cell proliferation, NF-κB activation and IL-1β production. These phenomena are known to be induced by physiological elevation of the oxidative state. Thus, these observations indicated that GPI-80 affects various tumor responses related to oxidation.
format article
author Yuji Takeda
Yuta Kurota
Tomoyuki Kato
Hiromi Ito
Akemi Araki
Hidetoshi Nara
Shinichi Saitoh
Nobuyuki Tanaka
Norihiko Tsuchiya
Hironobu Asao
author_facet Yuji Takeda
Yuta Kurota
Tomoyuki Kato
Hiromi Ito
Akemi Araki
Hidetoshi Nara
Shinichi Saitoh
Nobuyuki Tanaka
Norihiko Tsuchiya
Hironobu Asao
author_sort Yuji Takeda
title GPI-80 Augments NF-κB Activation in Tumor Cells
title_short GPI-80 Augments NF-κB Activation in Tumor Cells
title_full GPI-80 Augments NF-κB Activation in Tumor Cells
title_fullStr GPI-80 Augments NF-κB Activation in Tumor Cells
title_full_unstemmed GPI-80 Augments NF-κB Activation in Tumor Cells
title_sort gpi-80 augments nf-κb activation in tumor cells
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/a5810e6cad8b464db0454c85916ff062
work_keys_str_mv AT yujitakeda gpi80augmentsnfkbactivationintumorcells
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