Research Papers:
CD147 and downstream ADAMTSs promote the tumorigenicity of Kaposi’s sarcoma-associated herpesvirus infected endothelial cells
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Abstract
Lu Dai1,3, Jimena Trillo-Tinoco4, Yihan Chen1, Karlie Bonstaff3, Luis Del Valle4, Chris Parsons3, Augusto C. Ochoa5, Jovanny Zabaleta5, Bryan P. Toole6, Zhiqiang Qin1,2
1Research Center for Translational Medicine and Key Laboratory of Arrhythmias, East Hospital, Tongji University School of Medicine, Shanghai 200120, China
2Departments of Microbiology/Immunology/Parasitology, Louisiana State University Health Sciences Center, Louisiana Cancer Research Center, New Orleans, LA 70112, USA
3Department of Medicine, Louisiana State University Health Sciences Center, Louisiana Cancer Research Center, New Orleans, LA 70112, USA
4Department of Pathology, Louisiana State University Health Sciences Center, Louisiana Cancer Research Center, New Orleans, LA 70112, USA
5Department of Pediatrics, Louisiana State University Health Sciences Center, Louisiana Cancer Research Center, New Orleans, LA 70112, USA
6Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina and Hollings Cancer Center, Charleston, SC 29425, USA
Correspondence to:
Zhiqiang Qin, e-mail: [email protected]
Keywords: KSHV, Kaposi’s sarcoma, CD147, microarray
Received: August 26, 2015 Accepted: November 25, 2015 Published: December 12, 2015
ABSTRACT
Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiologic agent of several human cancers, including Kaposi’s sarcoma (KS), which preferentially arise in immunocompromised patients and lack effective therapeutic options. We have previously shown that KSHV or viral protein LANA up-regulates the glycoprotein CD147, thereby inducing primary endothelial cell invasiveness. In the current study, we identify the global network controlled by CD147 in KSHV-infected endothelial cells using Illumina microarray analysis. Among downstream genes, two specific metalloproteases, ADAMTS1 and 9, are strongly expressed in AIDS-KS tissues and contribute to KSHV-infected endothelial cell invasiveness through up-regulation of IL-6 and VEGF. By using a KS-like nude mouse model, we found that targeting CD147 and downstream ADAMTSs significantly suppressed KSHV-induced tumorigenesis in vivo. Taken together, targeting CD147 and associated proteins may represent a promising therapeutic strategy against these KSHV-related malignancies.
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