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E-GEOD-70594 - c-MET inhibitor inducing KSHV+ primary effusion lymphoma apoptosis

Released on 5 January 2016, last updated on 9 January 2016
Homo sapiens
Samples (6)
Array (1)
Protocols (7)
KSHV is a principal causative agent of primary effusion lymphoma (PEL). Despite this knowledge about the close relationship between HGF/c-MET network and solid tumors development, the role of HGF/c-MET in KSHV-related malignancies remains mostly unclear. We report that HGF/c-MET pathway is highly active within KSHV+ PEL cells and plays important role in tumor cell survival/growth. Targeting HGF/c-MET by a selective inhibitor, PF-2341066, significantly induces PEL apoptosis through a complex of underlying mechanisms, including cell-cycle arrest and DNA damage. By using microarray analysis, we have identified the global gene profile controlled by HGF/c-MET pathway within KSHV+ PEL cell-lines and several novel “druggable” candidates closely related to cancer cell survival/growth. Finally, we found that targeting HGF/c-MET pathway by PF-2341066 effectively prevents PEL tumor expansion and/or reduce established lymphoma progression in vivo. PEL cells were treated with vehicle control or c-MET inhibitor PF-2341066 (0.8 µM) for 24 h, and the gene expression signature was compared to respective vehicle controls
Experiment type
transcription profiling by array 
Zhiqiang Qin <>, Chris Parsons, Denise Whitby, Jimena Trillo-Tinoco, Jovanny Zabaleta, Karlie Bonstaff, Lu Dai, Luis Del Valle, Yueyu Cao
Targeting HGF/c-MET induces cell cycle arrest, DNA damage, and apoptosis for primary effusion lymphoma. Dai L, Trillo-Tinoco J, Cao Y, Bonstaff K, Doyle L, Del Valle L, Whitby D, Parsons C, Reiss K, Zabaleta J, Qin Z. , PMID:26531163
Investigation descriptionE-GEOD-70594.idf.txt
Sample and data relationshipE-GEOD-70594.sdrf.txt
Processed data (1)
Additional data (1)
Array designA-GEOD-10558.adf.txt