CRIP1 Reshapes the Gastric Cancer Microenvironment to Facilitate Development of Lymphatic Metastasis.
CRIP1
gastric cancer
lymphangiogenesis
lymphatic metastasis
Journal
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
ISSN: 2198-3844
Titre abrégé: Adv Sci (Weinh)
Pays: Germany
ID NLM: 101664569
Informations de publication
Date de publication:
09 2023
09 2023
Historique:
received:
19
05
2023
medline:
18
9
2023
pubmed:
6
7
2023
entrez:
6
7
2023
Statut:
ppublish
Résumé
Lymphangiogenesis in tumors provides an auxiliary route for cancer cell invasion to drainage lymph nodes, facilitating the development of lymphatic metastasis (LM). However, the mechanisms governing tumor lymphangiogenesis and lymphatic permeability in gastric cancer (GC) remain largely unknown. Here, the unprecedented role and mechanism of cysteine-rich intestinal protein-1 (CRIP1) in mediating the development of GC LM is uncovered. A series of assays are performed to identify downstream targets of CRIP1, and rescue experiments are performed to confirm the effects of this regulatory axis on LM. CRIP1 overexpression facilitates LM in GC by promoting lymphangiogenesis and lymphatic vessel permeability. CRIP1 promotes phosphorylation of cAMP responsive element binding protein 1(CREB1), which then mediates vascular endothelial growth factor C (VEGFC) expression necessary for CRIP1-induced lymphangiogenesis and transcriptionally promotes C-C motif chemokine ligand 5 (CCL5) expression. CCL5 recruits macrophages to promote tumor necrosis factor alpha (TNF-α) secretion, eventually enhancing lymphatic permeability. The study highlights CRIP1 regulates the tumor microenvironment to promote lymphangiogenesis and LM in GC. Considering the current limited understanding of LM development in GC, these pathways provide potential targets for future therapeutics.
Identifiants
pubmed: 37409440
doi: 10.1002/advs.202303246
pmc: PMC10502640
doi:
Substances chimiques
Vascular Endothelial Growth Factor C
0
CRIP1 protein, human
0
Carrier Proteins
0
LIM Domain Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2303246Subventions
Organisme : National Natural Science Foundation of China
ID : U1908207
Organisme : National Natural Science Foundation of China
ID : 81961128026
Organisme : National Natural Science Foundation of China
ID : 81872031
Organisme : National Natural Science Foundation of China
ID : 82172657
Organisme : National Natural Science Foundation of China
ID : 82202927
Organisme : China Postdoctoral Science Foundation
ID : 2022MD713824
Informations de copyright
© 2023 The Authors. Advanced Science published by Wiley-VCH GmbH.
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