Vesicular stomatitis virus infection triggers apoptosis associated with decreased Delta Np63 alpha and increased Bax levels in the immortalized HaCaT keratinocyte cell line

Megyeri, Klára and Orosz, László and Kemény, Lajos (2007) Vesicular stomatitis virus infection triggers apoptosis associated with decreased Delta Np63 alpha and increased Bax levels in the immortalized HaCaT keratinocyte cell line. BIOMEDICINE AND PHARMACOTHERAPY, 61 (5). pp. 254-260. ISSN 0753-3322

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Abstract

In view of the powerful inherent oncolytic activity exhibited by the vesicular stomatitis virus (VSV) in several tumor types, we set Put to investigate the susceptibility of the immortalized HaCaT keratinocyte cell line to VSV, and analyzed the role of apoptosis in the VSV-mediated induction of cell death. Indirect immunofluorescence assays, Western blot analyses and plaque titrations demonstrated that the HaCaT cell line was permissive to VSV replication. The results of ELISA for detection of the enrichment of nucleosomes in the cytoplasm of apoptotic cells revealed that VSV infection elicits the apoptotic death of HaCaT cells. Mock-infected HaCaT cells displayed the endogenous expression of Delta Np63 alpha, p53 mutated on UV hot spots (p53(mt)), Bcl-2 and p21 Bax. The levels of Delta Np63 alpha and p53(mt) were decreased, Bcl-2 remained unaffected, while the expressions of p21 Bax and p18 Bax were increased in VSV-infected HaCaT cells. Together, these data demonstrate that VSV replicates efficiently and triggers apoptosis in the immortalized HaCaT keratinocyte cell line. The VSV-mediated alterations in the expressions of Delta Np63 alpha and Bax may be implicated in the apoptotic responses of infected cells and may also sensitize to other apoptotic stimuli. These findings may stimulate further studies with the goal of developing VSV-based virotherapy into an effective modality for the treatment of epithelial-derived malignant tumors of the skin. (c) 2007 Elsevier Masson SAS. All rights reserved.

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