Non-Structural protein 1 (NS1) gene of Canine Parvovirus-2 regresses chemically induced skin tumors in Wistar rats
•We tested efficacy of Parvoviral NS1 gene to treat DMBA induced skin tumors in rats.•NS1 gene regresses skin tumors with no toxic effects on healthy cells.•NS1 treatment increases apoptosis but decreases mitotic index in skin tumors.•Also, NS1 promotes CD8+ and NK cell population to cause anti-tumo...
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Published in: | Research in veterinary science Vol. 97; no. 2; pp. 292 - 296 |
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Main Authors: | , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
Elsevier Ltd
01-10-2014
Elsevier Limited |
Subjects: | |
Online Access: | Get full text |
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Summary: | •We tested efficacy of Parvoviral NS1 gene to treat DMBA induced skin tumors in rats.•NS1 gene regresses skin tumors with no toxic effects on healthy cells.•NS1 treatment increases apoptosis but decreases mitotic index in skin tumors.•Also, NS1 promotes CD8+ and NK cell population to cause anti-tumor immune response.
The Non-Structural protein 1 of Canine Parvovirus-2 (CPV2.NS1) plays a major role in viral cytotoxicity and pathogenicity. CPV2.NS1 has been proven to cause apoptosis in HeLa cells in vitro in our laboratory. Here we report that CPV2.NS1 has no toxic side effects on healthy cells but regresses skin tumors in Wistar rats. Histopathological examination of tumor tissue from CPV2.NS1 treated group revealed infiltration of mononuclear and polymorphonuclear cells with increased extra cellular matrix, indicating signs of regression. Tumor regression was also evidenced by significant decrease in mitotic index, AgNOR count and PCNA index, and increase in TUNEL positive apoptotic cells in CPV2.NS1 treated group. Further, CPV2.NS1 induced anti-tumor immune response through significant increase in CD8+ and NK cell population in CPV2.NS1 treated group. These findings suggest that CPV2.NS1 can be a possible therapeutic candidate as an alternative to chemotherapy for the treatment of cancer. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0034-5288 1532-2661 |
DOI: | 10.1016/j.rvsc.2014.07.024 |