ABSTRACT
BACKGROUND: One of the most prevalent causes of cancer fatalities is hepatocellular carcinoma (HCC), which has been linked to metabolic syndrome. Circulating levels of the saturated fatty acid palmitate are elevated in metabolic syndrome and lead to cellular stress. MATERIALS AND METHODS: Using enzyme-linked immunosorbent assay, flow cytometry, and migration assays, we characterized the response of rat hepatoma cells to palmitate treatment. RESULTS: We detected a 60% increase in secretion of C-X-C motif ligand 1 (CXCL1) which was dose-dependent and coincided with apoptosis. We measured expression of C-X-C motif chemokine receptor 2 (CXCR2) and observed a 4.5-fold increase on apoptotic hepatoma cells. Furthermore, we assayed migration of hepatoma cells and saw a 2-fold increase in the number of migrating cells towards CXCL1. CONCLUSION: These findings suggest that HCC cells secrete CXCL1 in response to metabolic syndrome signals and may promote the progression of cancer through apoptosis recovery or metastasis.
