Carbonic anhydrase 13 suppresses bone metastasis in breast cancer.


Journal

Cancer treatment and research communications
ISSN: 2468-2942
Titre abrégé: Cancer Treat Res Commun
Pays: England
ID NLM: 101694651

Informations de publication

Date de publication:
2021
Historique:
received: 22 12 2020
revised: 02 02 2021
accepted: 05 02 2021
pubmed: 16 2 2021
medline: 4 1 2022
entrez: 15 2 2021
Statut: ppublish

Résumé

Metastatic progression is the leading cause of mortality in breast cancer. However, molecular mechanisms that govern this process remain unclear. In this study, we found that carbonic anhydrase 13 (CA13) plays a potential role in suppressing bone metastasis. iRFP713-labeled iCSCL-10A (iRFP-iCSCL-10A) breast cancer cells, which exhibit the hallmarks of cancer stem cells, exerted the ability of bone metastasis in hind legs after 5-week injections, whereas no metastasis was observed in control iRFP713-labeled MCF-10A (iRFP-MCF10A) cells. Transcriptome analysis indicated that the expression of several genes, including metabolism-related CA13, was reduced in bone metastatic iRFP-iCSCL-10A cells. In vitro and in vivo analyses demonstrated that overexpression of CA13 in iRFP-iCSCL-10A cells suppressed migration, invasion, and bone metastasis, together with the reduction of VEGF-A and M-CSF expression. Furthermore, we found that breast cancer patients with a low CA13 expression had significantly shorter overall survival and disease-free survival rates compared to those with higher CA13 expression. These findings suggest that CA13 may act as a novel prognostic biomarker and would be a therapeutic candidate for the prevention of bone metastasis in breast cancer.

Identifiants

pubmed: 33588197
pii: S2468-2942(21)00031-9
doi: 10.1016/j.ctarc.2021.100332
pii:
doi:

Substances chimiques

Biomarkers, Tumor 0
CSF1 protein, human 0
VEGFA protein, human 0
Vascular Endothelial Growth Factor A 0
Macrophage Colony-Stimulating Factor 81627-83-0
CA13 protein, human EC 4.2.1.1
Carbonic Anhydrases EC 4.2.1.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

100332

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Auteurs

Satomi Yogosawa (S)

Department of Biochemistry, The Jikei University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo 105-8461, Japan.

Jun Nakayama (J)

Division of Cellular Signaling, National Cancer Center Research Institute, Tokyo, Japan.

Mayuko Nishi (M)

Department of Microbiology, Yokohama City University School of Medicine, Yokohama, Japan.

Akihide Ryo (A)

Department of Microbiology, Yokohama City University School of Medicine, Yokohama, Japan.

Kiyotsugu Yoshida (K)

Department of Biochemistry, The Jikei University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo 105-8461, Japan. Electronic address: kyoshida@jikei.ac.jp.

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Classifications MeSH