Oncolytic HSV-1 Infection of Tumors Induces Angiogenesis and Upregulates CYR61
Open accessAbstract
Oncolytic viral therapy is under evaluation for toxicity and efficacy in clinical trials relating to several different tumors. We report a significant increase in the angiogenic index of oncolytic virus (OV)-treated glioma-matrigel implants (2.83-fold, P < 0.02). In a rat intracranial glioma model, large tumors from OV-treated animals were significantly more angiogenic than the phosphate-buffered saline (PBS)-treated control tumors (OV: 101 +/- 21.6; PBS: 19.8 +/- 10; P = 0.0037). Transcript profiling of OV-treated tumors revealed dysregulation of several transcripts involved in glioma angiogenesis. OV-mediated induction of CYR61 gene expression (8.94-fold, P = 0.001) correlated significantly with the presence of OV in tumor tissue in vivo (R = 0.7, P < 0.001). Further, induction of CYR61 mRNA and protein were confirmed in multiple human cancer cell lines and primary human tumor-derived cells in vitro, and in tumor lysate and cerebrospinal fluid (CSF) in vivo. Finally, we show that treatment of glioma cells with Cilengitide, known to counter CYR61-induced integrin activation, significantly suppressed the proangiogenic effect of OV treatment of gliomas (P < 0.05).
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CCN1 is induced by bacterial and viral infections and by inflammatory cytokines such as IL-1 and TNF-α.
“CCN1 is also induced by bacterial and viral infections [29–32], and by inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor α (TNF-α) [33].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [32]
CCN1 expression is induced by bacterial and viral infections.
“CCN1 expression is induced by inflammatory cytokines such as IL-1 and TNF-α [33,131], as well as by bacterial and viral infections [29–32].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [32]
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References 50 · Cited by 86
- Authors
- Kurozumi, K., Hardcastle, J., Thakur, R., Shroll, J., Nowicki, M., Otsuki, A., Chiocca, E. A., & Kaur, B.
- Affiliations
- The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (US)
- Corresponding author
- Kaur, Balveen
- Venue
- Molecular Therapy
- Publisher
- Elsevier BV
- Published
- 2008-08
- Volume
- 16
- Issue
- 8
- Pages
- 1382-1391
- ISSN
- 1525-0016 (ISSN-L)
- PMC
- PMC2659780
- OpenAlex
- W2106253728
- Cited by
- 86
- References
- 50
- Citations by year
- 2026: 1 · 2025: 5 · 2023: 2 · 2022: 8 · 2021: 4 · 2020: 6 · 2019: 4 · 2017: 4 · 2016: 2 · 2015: 5 · 2014: 4 · 2013: 9 · 2012: 8
- FWCI
- 4.38
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Molecular Therapy (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P01CA069246)
- National Institute of Neurological Disorders and Stroke (R01NS064607, R21NS056203, K01NS059575)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Virus-based gene therapy research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Oncology › Viral-associated cancers and disorders
- Keywords
- glioma, tumor angiogenesis, CYR61, cilengitide, integrin activation, oncolytic virotherapy, cerebrospinal fluid, gene expression profiling
- MeSH terms
- Animals, Glioma, Humans, Mice, Nude, Rats, Inbred F344, RNA, Messenger, Blotting, Western, Up-Regulation, Herpesvirus 1, Human, Neovascularization, Physiologic, Reverse Transcriptase Polymerase Chain Reaction, Xenograft Model Antitumor Assays, Cell Line, Tumor, Oncolytic Virotherapy, Mice, Rats, Cysteine-Rich Protein 61
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