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Tumor‐induced Factor (CXCL3) suppresses tumor initiation

Previously our lab uncovered a putative chemokine tumor‐induced factor (TIF) from a mouse xenograft model of copy number variation (CNV)‐mediated G protein‐coupled receptor (GPCR) MAS‐driven tumorigenesis. Sequence analysis and chemotactic study suggested that TIF was likely to be a hamster homolog of human GROγ (CXCL3) [IJC 125 (2009): 1316–1327]. Subsequently, genomic study of CHO‐K1 cells indicated that Tif gene consisted of 4 exons, characterized with an antisense B1 element which is embedded in the fourth exon (GenBank Accession No: EU293869). Two Tif transcripts were identified which shared identical sequences except that a string of 71‐nt derived from the antisense B1 element was deficient in the shorter transcript. By using the 71‐nt sequence as a probe, B1‐like RNA ladder was detected in xenografts. Pharmacological studies suggested that TIF activated Gi‐coupled CXCR2 and suppressed forskolin‐stimulated cAMP accumulation. In addition, TIF also induced calcium mobilization and ERK1/2 phosphorylation. Functional studies showed that TIF induced blood vessel formation and chemotaxis of CXCR2‐expressing cells. Overexpression of TIF in CHO‐K1 cells indicated that secreted mature TIF functioned as an autocrine factor and promoted anchorage‐independent growth. Unexpectedly, xenograft studies suggested that TIF delayed the onset of tumor formation but without exerting any inhibitory effect on tumor growth. These results suggest TIF suppresses tumor initiation and could be therapeutically valuable for preventing cancer relapse.