Modulation of autophagy affected tumorigenesis induced by the envelope glycoprotein of JSRV
View abstract on PubMed
Summary
This summary is machine-generated.Jaagsiekte sheep retrovirus (JSRV) causes ovine pulmonary adenocarcinoma (OPA) by manipulating autophagy. JSRV Env protein reduces autophagy markers, promoting tumor growth and metastasis.
Area Of Science
- Veterinary Pathology
- Molecular Biology
- Oncology
Background
- Ovine pulmonary adenocarcinoma (OPA) is a contagious lung tumor in sheep, caused by jaagsiekte sheep retrovirus (JSRV).
- OPA serves as an animal model for human lung adenocarcinomas, but the role of autophagy in its development is unclear.
Purpose Of The Study
- To investigate the role of autophagy in JSRV-induced ovine pulmonary adenocarcinoma.
- To determine how JSRV Env protein affects autophagic pathways during tumorigenesis.
Main Methods
- Western blotting to assess autophagy marker proteins (Beclin-1, LC3).
- Transmission electron microscopy and Cyto-ID dye staining to evaluate autophagosome formation.
- Mouse xenograft models to test the effect of autophagy inhibition on tumor growth.
Main Results
- Decreased expression of autophagy markers Beclin-1 and LC3 in OPA tissues and JSRV Env-expressing cells.
- Reduced autophagosome numbers in JSRV Env-expressing cells, with evidence of increased autolysosome degradation.
- Inhibition of autophagy suppressed tumor growth and epithelial-to-mesenchymal transition in mouse xenografts.
Conclusions
- JSRV Env protein dysregulates autophagy, contributing to OPA development.
- Autophagy modulation by JSRV is a key factor in ovine lung tumorigenesis.
- Targeting autophagy may offer a therapeutic strategy for OPA.
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