Peer-reviewed veterinary case report
Blocking KLF4 protein slows growth of dog mammary tumor cells
By Tien, Yung-Tien et al.·Published in Veterinary journal (London, England : 1997)·2015·Department and Graduate Institute of Veterinary Medicine·View original on PubMed →
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Original publication title: Downregulation of the KLF4 transcription factor inhibits the proliferation and migration of canine mammary tumor cells.
- Species:
- dog
Plain-English summary
A study found that a specific protein called KLF4 is linked to the growth and spread of mammary tumors in female dogs. When researchers used a treatment called Kenpaullone to lower KLF4 levels in these tumor cells, it slowed down their growth and movement, and even caused some of the cancer cells to die. This suggests that targeting KLF4 could be a promising approach for treating mammary tumors in dogs. If your dog has been diagnosed with a mammary tumor, discussing treatment options that focus on KLF4 might be worthwhile.
People also search for: dog mammary tumor treatment · KLF4 in dog cancer · Kenpaullone for canine tumors
Abstract
Canine mammary tumor (CMT) is the most common neoplasm in female dogs, and over 50% of CMTs are diagnosed as malignant. Krüppel-like factor 4 (KLF4) is a member of the KLF family of transcription factors and is associated with cell proliferation, differentiation, migration, and apoptosis. Although the role of KLF4 is still controversial in various human cancers, KLF4 has been identified as an oncogene in human breast cancer. Moreover, high KLF4 expression is correlated with an aggressive phenotype in CMT. Therefore, investigating the function of KLF4 may help better understand the pathogenesis of CMT. In this study, partial sequences of canine KLF4 and KLF4 expression were identified in various normal canine tissues, as well as CMT cells and Madin-Darby canine kidney (MDCK) cells. Kenpaullone, a small molecule inhibitor of KLF4, downregulated KLF4 expression in CMT cells and reduced CMT cell proliferation, migration, and colony formation in soft agar. Kenpaullone treatment induced S and G2/M phase arrest in CMT and MDCK cells, and induced death in CMT cells, but not in MDCK cells. It was concluded that KLF4 is expressed in various normal canine tissues, and downregulation of KLF4 inhibited CMT cell proliferation and migration, and induced cell death. The results of this study suggest that KLF4 may represent a suitable therapeutic target for CMT therapy.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/25616642/