Cell Research

Recent studies have shown that myeloid cells can make distant organs easily allow colony formation of spread tumor cell. However, the specific mechanism has been unknown. On May 14, Cancer Cell published a paper titled "S1PR1-STAT3 Signaling Is Crucial for Myeloid Cell Colonization at Future Metastatic Sites" to reveal its molecular mechanism. The researchers found that up-regulation of sphingosine-1 - phosphorylated receptor -1 (S1PR1)- STAT3 signaling pathway in the tumor cells, can increase S1PR1-STAT3 level in the targeted cell within tumor metastasis parts, resulting in the microenvironment that can easily accept metastatic tumour in distant tissues of the body. Inhibitiing function of S1PR1 or STAT3 in myeloid cells , we can undermine the existing microenvironment for easy transferation. Activation of S1PR1-STAT3 signaling pathway ,can ennable myeloid cells to pass through the blood vessels to form microenvironment that is conducive to tumor metastasis in distant organs , mediating continued survival and proliferation of their own and other stromal cells. Aafter analysis of cancer patients’lymph nodes that contain none tumor cells, compared with normal lymph node cells, tumor specimens of patients showed higher myeloid-like cell infiltration, high level activation of STAT3 and enhancements of cell survival signal.