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Many cancers express an array of chemokines which have the capacity to modulatethe nature and function of intratumoural leukocyte infiltrates. In malignant mesothelioma(MM) neither the chemokine signalling networks nor their regulation have beeninvestigated despite the prominence of leucocytic infiltrates in both clinicaland experimental tumours. In this study, we examined constitutive and cytokine-regulatedexpression of CC and CXC chemokine genes in mesothelioma and mesothelial cellcultures derived from two different mouse strains (BALB/C and CBA/CaH). In mouseMM and mesothelial cells MCP-1/JE, GRO-α/KC and RANTES were expressed whereasMIP-1α and MIP-2 were infrequently expressed. Comparison of basal chemokine expressionshowed that GRO-α/KC mRNA was overexpressed in the malignant cells whereas MCP-1gene expression and release was downregulated. Treatment of mesothelioma cellswith IL-4, IFN-γ or TNF-α revealed that chemokine genes could be more responsiveto cytokines in the malignant compared to their mesothelial cells. TNF-α was consistentlythe most potent positive regulator of both CC and CXC chemokine expression andMCP-1 release. The present study for the first time provides a mechanistic insightinto the differential regulation of chemokine expression in malignant mesotheliomacells and has implications for mesothelial chemokine signalling in mouse models.

Regulated chemokine gene expression in mouse mesothelioma and mesothelial cells: TNF-α upregulates both CC and CXC chemokine genes