IFI35 Promotes Renal Cancer Progression by Inhibiting pSTAT1/pSTAT6-Dependent Autophagy.
IFI35
RCC
autophagy
diagnostic biomarker
renal cancer
therapeutic target
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
09 Jun 2022
09 Jun 2022
Historique:
received:
15
03
2022
revised:
06
06
2022
accepted:
07
06
2022
entrez:
24
6
2022
pubmed:
25
6
2022
medline:
25
6
2022
Statut:
epublish
Résumé
Interferon-induced protein 35 (IFI35), is currently acknowledged to govern the virus-related immune inflammatory responses. However, the biological significance and function of IFI35 in renal cell cancer (RCC) is still not well understood. Here, IFI35 expression and function were investigated in RCC tissues, renal cancer cells, and animal models. The results showed that IFI35 expression was significantly increased in 200 specimens of RCC patients. We found that higher IFI35 levels were significantly correlated with poor RCC prognosis. In human cell lines, the knockdown of IFI35 suppressed the malignant behavior of renal cancer cells. Similarly, the IFI35 knockdown resulted in significant inhibition of tumor progression in the subcutaneous or lung metastasis mouse model. Furthermore, the knockdown of IFI35 promoted the induction of autophagy by enhancing the autophagy-related gene expression (LC3-II, Beclin-1, and ATG-5). Additionally, blockade of STAT1/STAT6 phosphorylation (pSTAT1/pSTAT6) abrogated the induced autophagy by IFI35 knockdown in renal cancer cells. The autophagy inhibitor 3-MA also abolished the prevention of tumor growth by deleting IFI35 in renal cancer models. The above results suggest that the knockdown of IFI35 suppressed tumor progression of renal cancer by pSTAT1/pSTAT6-dependent autophagy. Our research revealed that IFI35 may serve as a potential diagnosis and therapeutic target for RCC.
Identifiants
pubmed: 35740527
pii: cancers14122861
doi: 10.3390/cancers14122861
pmc: PMC9221357
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : National Natural Science Foundation of China
ID : 82072814, 81702499
Organisme : Jiangsu Province Natural Science Foundation
ID : BK20170266
Organisme : Natural Science Fund for Colleges and Universities in Jiangsu Province
ID : 19KJB310001
Organisme : Qing Lan Project of Jiangsu Province, Youth Technology Innovation Team of Xuzhou Medical University
ID : TD202003
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