Abstract

Abstract Thyroid hormones(THs) are multi-function mediators that modulate various physiological processes. Thyroid hormone receptors(TRs) are type II nuclear receptors, TRs binds to thyroid hormone response elements (TREs) of target promoter regions modulates target gene expression at the transcriptional level upon THs binding. Previous literatures illustrate an association between aberrant TR regulation and human hepatocellular carcinoma (HCC). We employed cDNA microarrays and SILAC secretome analysis to identify the T3-regulated secreted proteins after T3 treatment in TR-expressing hepatoma cell lines, Chemokine (C-C motif) ligand 16 (CCL16) expression is positively regulated by T3 treatment. The patients with higher expression of CCL16 have poor recurrence survival rate. Ectopic expression of CCL16 in HCC cell lines increased tumor growth rate in vivo but not in vitro. CCL16 induced chemotaxis of monocytes and macrophages via interacting with its receptors CCR1 and CCR5. Expression of proangiogenic genes in macrophages were increased while co-cultured with HCC cell lines. The motility of HUVECs were increased after treated with conditional medium of macrophages co-cultured with HCC cell lines. Our study revealed that CCL16 recruited macrophage and promoted tumor progression. Citation Format: Cheng-Heng Wu, Kwang-Huei Lin. The biological significance of CCL 16 regulated by thyroid hormone in liver cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5206.

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