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AssigneeBoard of Regents, The University of Texas System
InventorsUsha R. Pendurthi, Vijaya M. R. Lella, Shivakeshava Gaddam, Steven Idell
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The influence of TF, endothelial cell protein C receptor (EPCR) and protease activated receptor-1 (PAR1) on tumor growth of malignant pleural mesothelioma (MPM) is disclosed. MPM cells that lack or express TF, EPCR or PAR1 and a murine orthotopic model of MPM led to the discovery that intrapleural administration into nude mice of REN MPM cells expressing TF and PAR1 but lacking EPCR and PAR2 generated large pleural cavity tumors. Suppression of TF or PAR1 expression markedly reduced tumor growth. Overexpression of TF in non-aggressive MPM cells expressing EPCR and PAR1 but exhibiting minimal levels of TF failed to alter their tumorigenicity. Introduction of EPCR expression in aggressive MPM cells attenuated tumor growth whereas EPCR silencing in non-aggressive MPM cells overexpressing TF increased tumorigenicity of non-aggressive cells. Expression of EPCR by MPM cells suppresses tumor growth and treats MPM.
A method of sensitizing malignant pleural mesothelioma (MPM) cells to killing by endogenous cytokines in a subject in need thereof, said method comprising transducing MPM cells to express Endothelial Protein C Receptor (EPCR), by exposing them to a nucleic acid expression vector, wherein said vector is administered intrapleurally to said subject, the vector comprising a nucleotide sequence comprising:
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