Abstract
G A A b st ra ct s induced. To investigate the role of ST2 in vivo, CT26ST2 shRNA cells were injected subcutaneously into BALB/C mice. Knockdown of ST2 in colon tumours resulted in enhanced tumour growth (2.3 fold increase compared to CT26scr shRNA) in vivo. This was confirmed using three separate clones, andwas associatedwith alterations in immune cell infiltration, including a decrease in macrophage and cytotoxic T cell numbers. Characterization of human colon tumours ex vivo revealed that both normal and neoplastic cells expressed ST2L. However, neoplastic cells showed significantly reduced expression of ST2L as compared to adjacent non-tumour tissue as assessed by qRT-PCR, protein and immunohistochemistry. In addition expression of ST2Lwas found to decrease with increasing tumour grade with lower expression of ST2L and to correlate with poor prognosis. No change was observed for serum IL-33 or sST2 levels. Conclusions: Our results indicate that the IL-33/ST2 signalling axis may play a protective role in colon carcinogenesis, possibly due to potent recruitment of macrophages by IL-33 signalling. Further studies are required to determine whether manipulation of this pathway represents a potential therapeutic target.
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