Matricellular Protein WISP2 Is an Endogenous Inhibitor of Collagen Linearization and Cancer Metastasis.
Animals
Apoptosis
Biomarkers, Tumor
/ genetics
Breast Neoplasms
/ metabolism
CCN Intercellular Signaling Proteins
/ antagonists & inhibitors
Cell Movement
Cell Proliferation
Collagen Type I
/ antagonists & inhibitors
Female
Gene Expression Regulation, Neoplastic
Humans
Lung Neoplasms
/ metabolism
Mice
Mice, Inbred BALB C
Mice, Inbred NOD
Mice, Nude
Mice, SCID
Neoplasm Invasiveness
Prognosis
Proto-Oncogene Proteins
/ antagonists & inhibitors
Repressor Proteins
/ genetics
Signal Transduction
Survival Rate
Tumor Cells, Cultured
Xenograft Model Antitumor Assays
Journal
Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R
Informations de publication
Date de publication:
15 11 2021
15 11 2021
Historique:
received:
29
11
2020
revised:
06
07
2021
accepted:
11
08
2021
pubmed:
14
8
2021
medline:
11
1
2022
entrez:
13
8
2021
Statut:
ppublish
Résumé
Collagen remodeling contributes to many physiologic and pathologic processes. In primary tumors, the linearization of collagen fibers promotes cancer cell invasion and metastasis and is indicative of poor prognosis. However, it remains unknown whether there are endogenous inhibitors of collagen linearization that could be exploited therapeutically. Here, we show that collagen linearization is controlled by two secreted matricellular proteins with antagonistic functions. Specifically, WISP1 was secreted by cancer cells, bound to type I collagen (Col I), and linearized Col I via its cysteine-rich C-terminal (CT) domain. In contrast, WISP2, which lacks a CT domain, inhibited Col I linearization by preventing WISP1-Col I binding. Analysis of patient data revealed that
Identifiants
pubmed: 34385183
pii: 0008-5472.CAN-20-3982
doi: 10.1158/0008-5472.CAN-20-3982
pmc: PMC8595651
mid: NIHMS1734778
doi:
Substances chimiques
Biomarkers, Tumor
0
CCN Intercellular Signaling Proteins
0
CCN4 protein, human
0
CCN5 protein, human
0
Collagen Type I
0
Proto-Oncogene Proteins
0
Repressor Proteins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
5666-5677Subventions
Organisme : NCI NIH HHS
ID : P30 CA021765
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA245301
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
©2021 American Association for Cancer Research.
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