Abstract 3758: RIG-I plays a critical role in negatively regulating stemness properties in hepatoma cell lines.

Abstract

Abstract Hepatocellular carcinoma (HCC) is the third most common cause of death from cancer worldwide due to its high rate of recurrence. Cancer stem cells are considered to generate tumors through the stem cell processes including self-renewal and differentiation into multiple cell types. And these distinct populations of cells are suggested to cause relapse and metastasis by eliciting new tumors. Retinoic acid-inducible gene I (RIG-I) has been identified as a pattern recognition receptor in innate immune defense for sensing intracellular viral RNAs, like Hepatits C virus which is one of the major risks of HCC, and inducing type I interferons production. In previous studies, RIG-I-like receptors recognizing some potentially oncogenic agents may have functional consequences that can lead to association of such single nucleotide polymorphisms with risk of some diseases or even cancers. Thus these gene polymorphisms may affect cancer risk indirectly. On the other hand, a previous study have demonstrated that RIG-I is an essential regulator of physiological myelopoiesis suggesting RIG-I possesses the potential of modulating stem cell differentiation. In our present study, we examined Huh7 and its RIG-I-mutant cell line by sphere formation assay and found solely the mutated cells possessed the self-renewal ability. After transfection of dominant-negative mutant of RIG-I to Huh7, the self-renewal ability were rescued as expected. We also injected 1000 cells for each two cell lines into NOD/SCID mice subcutaneously and observed the mutated cells formed tumors whereas Huh7 didn't. Hence, our study reveals the potential of RIG-I to suppress the stemness properties in the HCC cell lines and provides a new possible remedy target of liver cancer. Citation Format: Ping-Yu Chen, Chao-Kuen Lai, Min-Linag Kuo. RIG-I plays a critical role in negatively regulating stemness properties in hepatoma cell lines. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3758. doi:10.1158/1538-7445.AM2013-3758