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Metastasis is a major cause of cancer mortality. We generated an autochthonous transgenic mouse model whereby conditional expression of  MYC  and  Twist1  enables hepatocellular carcinoma (HCC) to metastasize in &gt;90% of mice.  MYC  and  Twist1  cooperate and their sustained expression is required to elicit a transcriptional program associated with the activation of innate immunity, through secretion of a cytokinome that elicits recruitment and polarization of tumor associated macrophages (TAMs). Systemic treatment with Ccl2 and Il13 induced  MYC -HCCs to metastasize; whereas, blockade of Ccl2 and Il13 abrogated  MYC / Twist1 -HCC metastasis. Further, in 33 human cancers (n = 9502)  MYC  and  TWIST1  predict poor survival (p=4.3×10 −10 ), CCL2/IL13 expression (p&lt;10 −109 ) and TAM infiltration (p&lt;10 −96 ). Finally, in the plasma of patients with HCC (n = 25) but not cirrhosis (n = 10), CCL2 and IL13 were increased and IL13 predicted invasive tumors. Therefore,  MYC  and  TWIST1  generally appear to cooperate in human cancer to elicit a cytokinome that enables metastasis through crosstalk between cancer and immune microenvironment.

MYC and Twist1 cooperate to drive metastasis by eliciting crosstalk between cancer and innate immunity