TSG-6 promotes Cancer Cell aggressiveness in a CD44-Dependent Manner and Reprograms Normal Fibroblasts to create a Pro-metastatic Microenvironment in Colorectal Cancer.
Animals
Cancer-Associated Fibroblasts
/ metabolism
Cell Line, Tumor
Cell Movement
/ genetics
Colorectal Neoplasms
/ metabolism
Epithelial-Mesenchymal Transition
/ genetics
Fibroblasts
/ metabolism
Gene Expression Regulation, Neoplastic
Signal Transduction
/ genetics
Tumor Microenvironment
/ genetics
Colorectal Cancer
Fibroblast
Metastasis
TSG-6
Journal
International journal of biological sciences
ISSN: 1449-2288
Titre abrégé: Int J Biol Sci
Pays: Australia
ID NLM: 101235568
Informations de publication
Date de publication:
2022
2022
Historique:
received:
17
11
2021
accepted:
21
01
2022
entrez:
14
3
2022
pubmed:
15
3
2022
medline:
16
4
2022
Statut:
epublish
Résumé
Tumor necrosis factor α stimulated gene 6 (TSG-6), a 30-KD secretory protein, plays an essential role in modulating inflammatory responses and extracellular matrix remodeling. However, little is known regarding the role of TSG-6 in human cancers. Here, we investigated the mechanism of action and the role of TSG-6 in colorectal cancer (CRC) metastasis. We found that TSG-6 was highly expressed in tumor tissues and was associated with poor prognosis and metastasis in CRC. Mechanistically, TSG-6 overexpression in CRC cells resulted in ERK activation and epithelial-mesenchymal transition by means of stabilizing CD44 and facilitating the CD44-EGFR complex formation on the cell membrane. Consequently, this resulted in the promotion of tumor migration and invasion both
Identifiants
pubmed: 35280699
doi: 10.7150/ijbs.69178
pii: ijbsv18p1677
pmc: PMC8898369
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1677-1694Informations de copyright
© The author(s).
Déclaration de conflit d'intérêts
Competing Interests: The authors have declared that no competing interest exists.
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