Host inflammatory cells are recruited to tumor sites and contribute to tumor progression. Myeloid Immune Suppressor Cell (MISC) is one such cell type involved in this process. The deletion of TGF-Beta type II receptor (TGF-β rII) in mammary tumor virus-polyomavirus middle T antigen (MMTV-PyVmT) transgenic mice showed shortened tumor latency and decreased survival. Interestingly, increased number of MISCs was found in tumors derived from MMTV-PyVmT TGF-β rII ko mice. This suggests that deletion of TGF-β is involved in the recruitment of MISCs in mammary tumors. The goal of this study was to 1) investigate the recruitment of MISCs to TGF-β rII ko breast tumors by chemokine CXCL5 and 2) understand the role of MISCs in tumor progression and metastasis. Preliminary data indicate an increased CXCL5 production in TGF-β rII ko tumors when compared with controls, a possible mechanism for the recruitment of MISCs. We are currently using western blots and ELISAs to confirm this result. MISCs in tumor microenvironments must provide certain advantages for tumors to progress. Using real time PCR (rtPCR), we found MISCs in tumor microenvironments produce metalloproteinase (MMPs), important enzymes in degrading cellular matrix for tumors to invade. In addition, 4T1 breast cancer cells co-cultured with MISCs form significantly more colonies in Anchorage Independent Colony Formation Assays. Together, these data suggest MISCs contribute to tumor progression and metastasis by providing degrading enzymes and helping establish metastasis colonies. Understanding the recruitment of MISCs to tumor sites and their impact on tumor progression could lead to new opportunities for anti-cancer treatments in the near future.

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