The EGFR Macrophage promotes liver cancer
Hepatocellular carcinoma (HCC) is a common cancer with limited treatment options and poor prognosis. Tumorigenesis has been associated with chronic inflammation mediated by macrophages and different signaling pathways, including the receptor for epidermal growth factor (EGFR) track. The precise role of EGFR in HCC is unknown, and EGFR inhibitors have shown disappointing clinical results. Here, we found that EGFR is expressed in macrophages in both human liver and HCC in a
mouse model of HCC. Mice lacking EGFR show in hepatocarcinogenesis
alteration macrophages, whereas mice lacking hepatocyte EGFR develop HCC more
unexpectedly due to increased damage and compensatory proliferation of
hepatocytes. Mechanically, interleukin-1, upon stimulation, the EGFR necessary
liver macrophages to induce transcription of the interleukin-6, which triggers
the proliferation of hepatocytes and HCC. Importantly, the presence of
EGFR-positive hepatic macrophages in patients with HCC is associated with poor
survival. This study shows a mechanism of tumor promotion not EGFR in tumor
cells, which could lead to more effective strategies of drug accuracy.
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