Peer-reviewed veterinary case report
Propranolol helps virus kill canine mammary tumor cells better
By Zhu, Yunjie et al.·Published in The veterinary quarterly·2026·Department of Veterinary Clinical Sciences, China·View original on PubMed →
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Original publication title: Propranolol enhances the oncolytic effect of newcastle disease virus on canine mammary tumor cell by modulating the IFN-I-mediated JAK-STAT signaling pathway.
- Species:
- dog
Plain-English summary
A study found that propranolol, a medication commonly used for heart issues, may help treat canine mammary tumors (CMT) in female dogs by improving the effectiveness of a virus called Newcastle disease virus (NDV). This combination therapy worked by allowing the virus to replicate better and attack the tumor cells more effectively. In tests, both NDV alone and the combination with propranolol helped slow down tumor growth and extended survival in dogs with CMT. This suggests that using propranolol alongside NDV could be a promising new treatment option for this type of cancer in dogs.
People also search for: dog mammary tumor treatment · propranolol for canine cancer · Newcastle disease virus in dogs
Abstract
Canine mammary tumors (CMT), the most common neoplasms in intact female dogs, lack effective treatments for advanced cases. Newcastle disease virus (NDV), an oncolytic virus, kills tumor cells directly and stimulates antitumor immunity. However, NDV also activates Type I interferon (IFN-I) signaling, which restricts its replication via the JAK-STAT pathway. This study investigated whether propranolol, known to suppress antiviral responses, could enhance NDV's oncolytic effect in CMT., using the CMT-U27 cell line, the combination reduced cell viability, migration, and invasion. Propranolol increased NDV replication and suppressed NDV-induced IFN-I release and JAK-STAT signaling pathway activation. In the CMT-U27 xenograft model, both NDV alone and the combination therapy prolonged the survival and suppressed tumor growth, with no significant difference between the two. However, the combination markedly enhanced intratumoral NDV replication by inhibiting IFN-I production and the JAK-STAT signalling pathway. These findings indicate that propranolol enhances NDV-mediated oncolysis in CMT by inhibiting the IFN-I/JAK-STAT pathway, increasing viral load, and represents a promising combined therapeutic strategy.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/41866332/