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CCL9 Mediates TGF-β Regulation of Tumor Cell Survival and Lung Metastasis

Wednesday, October 10, 2012 — Poster Session II

Noon – 2:00 p.m

Natcher Conference Center, Building 45




  • HH Yan
  • Y Pang
  • L Yang


Cancer metastasis is an ominous feature of tumor progression and accounts for over 90% of cancer-associated deaths. Tumor cell survival in the distant organ is the rate-limiting step in the metastatic process. Primary tumors modulate the pre-metastatic organs and build up a tumor favorable “soil” for the “seeds” (tumor cells). However, the precise cellular and molecular mechanisms remain to be elucidated. We found that Gr-1+CD11b+ cells or myeloid derived suppressor cells (MDSCs) infiltrate and landscape the pre-metastatic lung into an inflammatory, proliferative, and immune suppressive environment. Tumor cells co-cultured or co-injected with MDSCs showed increased survival and metastasis. Using a cytokine protein array screening, we found that CCL9 (MIP1-Υ, macrophage inflammatory protein-1 gamma) is highly secreted in the supernatant of co-culture as well as the metastatic lung. We identified that MDSCs is the main source for CCL9 expression. Interestingly, deletion of transforming growth factor -β receptor II (TβRII) in myeloid cells, results in significantly decreased lung metastasis and CCL9 expression. We are currently investigating how CCL9 affect tumor cell survival and metastasis.

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