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Felis catus papillomavirus type 2 E6 oncogene enhances mitogen-activated protein kinases and Akt activation but not EGFR expression in an in vitro feline model of viral pathogenesis. | LitMetric

AI Article Synopsis

  • Recent research suggests that Felis catus papillomavirus type 2 (FcaPV2) may contribute to the development of feline oral and skin cancers by showing viral gene activity in live animals and oncogenic properties in lab tests.
  • The study found that the presence of the FcaPV2 E6 protein in feline cells leads to increased levels of important signaling molecules (pMEK, pERK, and pAkt), which are key regulators of cell growth and survival, thereby promoting tumor formation.
  • Unlike human papillomavirus-associated tumors, the activation of these signaling pathways in cats does not rely on changes in the epidermal growth factor receptor (EGFR), indicating a different molecular mechanism in feline cancers.

Article Abstract

A possible causative role of Felis catus papillomavirus type 2 (FcaPV2) in the development of feline oral and cutaneous squamous cell carcinomas (SCC) has been recently suggested by demonstrating viral gene expression in vivo and transforming properties by its putative oncogenes E6 and E7 in vitro. The activated molecules MEK (pMEK), ERK (pERK) and Akt (pAkt) are signaling transduction effectors regulating cell proliferation and inhibition of apoptosis, which are critical steps towards tumour formation. Here, we show by Western blotting (WB) that expression of FcaPV2 E6 in feline epithelial cells enhances pMEK, pERK and pAkt levels compared to control cells. Additionally, we demonstrated by real-time quantitative PCR on epidermal growth factor receptor (EGFR) transcripts and WB that activation of these signaling routes is independent from EGFR differential gene expression, total protein levels or phosphorylation, unlike in human papillomavirus associated tumours. This study contributes to define the molecular scenario underlying FcaPV2-triggered pathogenesis of feline SCC.

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Source
http://dx.doi.org/10.1016/j.vetmic.2016.09.013DOI Listing

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