期刊
CANCER CELL
卷 11, 期 3, 页码 245-258出版社
CELL PRESS
DOI: 10.1016/j.ccr.2007.01.015
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资金
- NATIONAL CANCER INSTITUTE [R01CA109232, R01CA124332, R01CA163217, R01CA075918, R01CA096512, R03CA110136, R01CA132637] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE018304] Funding Source: NIH RePORTER
- NCI NIH HHS [CA075918, R03 CA110136, R01 CA109232, R01 CA163217, R01 CA096512, R01 CA124332, R01 CA075918, R01 CA132637, R01 CA109232-05, CA109232, CA110136, CA096512] Funding Source: Medline
- NIDCR NIH HHS [R01 DE018304-02, R01 DE018304-03, R01 DE018304, R01 DE018304-01] Funding Source: Medline
Transfection of a Kaposi's sarcoma (KS) herpesvirus (KSHV) Bacterial Artificial Chromosome (KSHVBac36) into mouse bone marrow endothelial-lineage cells generates a cell (mECK36) that forms KS-like tumors in mice. mECK36 expressed most KSHV genes and were angiogenic, but they didn't form colonies in soft agar. In nude mice, mECK36 formed KSHV-harboring vascularized spindle cell sarcomas that were LANA+/podoplanin+, overexpressed VEGF and Angiopoietin ligands; and receptors, and displayed KSHV and host transcriptomes reminiscent of KS. mECK36 that lost the KSHV episome reverted to nontumorigenicity. siRNA suppression of KSHV vGPCR, an angiogenic gene upregulated in mECK36 tumors, inhibited angiogenicity and tumorigenicity. These results show that KSHV malignancy is in vivo growth restricted and reversible, defining mECK36 as a biologically sensitive animal model of KSHV-dependent KS.
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