Do PPAR𝛾 Ligands Suppress the Growth of Cholangiocarcinoma or the Cholangiohepatitis Induced by the Tumor?

Figure 1

Inhibitory effects of PPARγ ligand on the development of cholangiocarcinoma. PPARγ ligand directly suppresses tumor progression through p53 and Smad pathways (red arrow) and also stimulates adipocyte and hepatobiliary cells (gray arrow). Secretion of adipokines (TNF-α, adiponectin, and leptin) and production of lipid-related proteins (FABP and LPL) are regulated by PPARγ ligand. Up- and downregulation of various gene signals from adipocytes (yellow line) and hepatobiliary cells (broken line) promoted suppression of tumor growth. As a result, PPARγ indirectly suppressed tumor growth of cholangiocarcinoma through adipocytes and hepatobiliary cells. Currently, evidence of suppressive signals from hepatobiliary cells to cholangiocarcinoma is unavailable (broken line). FABP: fatty acid binding protein, LPL: lipoprotein lipase, TNF-α: tumor necrosis factor-α.