Infection and chronic inflammation contribute to about 1 in 4 of all cancer cases. Emerging evidence suggests that the host factors in the tumor microenvironment may interact with underlying inflammatory prostate cancer cells to make them aggressive. In this study, we hypothesized that soluble factors secreted by immune cells activated by inflammation can induce EMT in prostate cancer and thus promote metastasis. We identify that macrophage-secreted cytokines including TNFα act as mediators for potentiating LNCaP cell proliferation in migration assay. Hence, our data indicate a mechanistic insight of how inflammation may contribute to development of prostatic disease at an early stage through increasing cell proliferation and metastasis of LNCaP cells
