Abstract

Hepatocellular cancer (HCC) progression requires activation of the tumor-stromal microenvironment. Polarized tumor-associated macrophages with M2-like phenotype (TAM2) represent a critical pro-tumor component in this niche. The mechanisms that regulate TAM2 in HCC remain poorly characterized. Recently, tumor-derived osteopontin (OPN) has been shown to be significantly expressed in HCC. We hypothesize that TAM2 are critical to OPN-dependent signaling and they significantly enhance HCC invasion.

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