TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment.
Animals
Apoptosis
Cell Movement
Cell Proliferation
Female
Gene Expression Regulation, Neoplastic
Humans
Mice
Mice, Inbred C57BL
Neoplasm Invasiveness
Pancreatic Neoplasms
/ genetics
Tripartite Motif Proteins
/ genetics
Tumor Cells, Cultured
Tumor Microenvironment
Ubiquitin-Protein Ligases
/ genetics
Xenograft Model Antitumor Assays
TRIM37
immune microenvironment
pancreatic cancer
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
21 Jan 2022
21 Jan 2022
Historique:
received:
31
10
2021
revised:
19
01
2022
accepted:
19
01
2022
entrez:
15
2
2022
pubmed:
16
2
2022
medline:
5
3
2022
Statut:
epublish
Résumé
TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migration, and invasion ability of pancreatic cancer cells. Furthermore, an in vivo study using an orthotopic syngeneic animal model further confirmed that reduced expression of TRIM37 in cancer cells suppressed tumor growth in vivo. Moreover, in mice bearing TRIM37 knockdown pancreatic cancer cells, the proportion of CD11b
Identifiants
pubmed: 35163097
pii: ijms23031176
doi: 10.3390/ijms23031176
pmc: PMC8835669
pii:
doi:
Substances chimiques
Tripartite Motif Proteins
0
TRIM37 protein, human
EC 2.3.2.27
Ubiquitin-Protein Ligases
EC 2.3.2.27
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : China Medical University Hospital Taiwan
ID : DMR-107-033
Organisme : China Medical University Taiwan
ID : CMU103-S-27
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