Oxidized high mobility group B-1 enhances metastability of colorectal cancer via modification of mesenchymal stem/stromal cells.
HMGB1
cancer metastasis
colorectal cancer
mesenchymal stem cell
stemness
Journal
Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776
Informations de publication
Date de publication:
Aug 2022
Aug 2022
Historique:
revised:
28
04
2022
received:
06
01
2022
accepted:
10
05
2022
pubmed:
17
5
2022
medline:
10
8
2022
entrez:
16
5
2022
Statut:
ppublish
Résumé
High mobility group box-1 (HMGB1) is known to be a chemotactic factor for mesenchymal stem/stromal cells (MSCs), but the effect of post-translational modification on its function is not clear. In this study, we hypothesized that differences in the oxidation state of HMGB1 would lead to differences in the function of MSCs in cancer. In human colorectal cancer, MSCs infiltrating into the stroma were correlated with liver metastasis and serum HMGB1. In animal models, oxidized HMGB1 mobilized three-fold fewer MSCs to subcutaneous tumors compared with reduced HMGB1. Reduced HMGB1 inhibited the proliferation of mouse bone marrow MSCs (BM-MSCs) and induced differentiation into osteoblasts and vascular pericytes, whereas oxidized HMGB1 promoted proliferation and increased stemness, and no differentiation was observed. When BM-MSCs pretreated with oxidized HMGB1 were co-cultured with syngeneic cancer cells, cell proliferation and stemness of cancer cells were increased, and tumorigenesis and drug resistance were promoted. In contrast, co-culture with reduced HMGB1-pretreated BM-MSCs did not enhance stemness. In an animal orthotopic transplantation colorectal cancer model, oxidized HMGB1, but not reduced HMGB1, promoted liver metastasis with intratumoral MSC chemotaxis. Therefore, oxidized HMGB1 reprograms MSCs and promotes cancer malignancy. The oxidized HMGB1-MSC axis may be an important target for cancer therapy.
Identifiants
pubmed: 35570394
doi: 10.1111/cas.15400
pmc: PMC9357642
doi:
Substances chimiques
HMGB1 Protein
0
HMGB1 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2904-2915Subventions
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 19K16564
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 20K11260
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 20K19349
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 20K21659
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 21K10143
Informations de copyright
© 2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
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