RABL6A Promotes Pancreatic Neuroendocrine Tumor Angiogenesis and Progression In Vivo.
RABL6A
RIP-Tag2 mouse model
angiogenesis
c-Myc
pancreatic neuroendocrine tumors
Journal
Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304
Informations de publication
Date de publication:
02 Jun 2021
02 Jun 2021
Historique:
received:
27
04
2021
revised:
26
05
2021
accepted:
28
05
2021
entrez:
2
7
2021
pubmed:
3
7
2021
medline:
3
7
2021
Statut:
epublish
Résumé
Pancreatic neuroendocrine tumors (pNETs) are difficult-to-treat neoplasms whose incidence is rising. Greater understanding of pNET pathogenesis is needed to identify new biomarkers and targets for improved therapy. RABL6A, a novel oncogenic GTPase, is highly expressed in patient pNETs and required for pNET cell proliferation and survival in vitro. Here, we investigated the role of RABL6A in pNET progression in vivo using a well-established model of the disease. RIP-Tag2 (RT2) mice develop functional pNETs (insulinomas) due to SV40 large T-antigen expression in pancreatic islet β cells. RABL6A loss in RT2 mice significantly delayed pancreatic tumor formation, reduced tumor angiogenesis and mitoses, and extended survival. Those effects correlated with upregulation of anti-angiogenic p19ARF and downregulation of proangiogenic
Identifiants
pubmed: 34199469
pii: biomedicines9060633
doi: 10.3390/biomedicines9060633
pmc: PMC8228095
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : NCI NIH HHS
ID : P30 CA086862
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA260200
Pays : United States
Organisme : NCI NIH HHS
ID : NET SPORE P50 CA174521
Pays : United States
Organisme : NCI NIH HHS
ID : Core Grant P30 CA086862
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA174521
Pays : United States
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