Abstract 4177: Detection of mir-449 and mir-let-7g expression in Taiwan paired hepatocellular carcinoma.

Abstract Hepatocellular carcinoma (HCC) is one of the most common and rapidly fatal human malignancies. In recent decades, it has been increasing in Western, developed countries such as the United States. MicroRNAs (miR) regulate genes involved in diverse biological functions and alterations in miR expression have been linked to the pathogenesis of many malignancies. Some previous studies have reported that miR-449 and miR-let-7g have tumor suppressor functions, but other studies indicate that miR-449 may have more variable functions. In the present study, miR-449 and miR-let-7g expression were measured in 36 Taiwanese paired HCC tumor/adjacent tissues using formalin fixed paraffin embedded samples with real-time RT-PCR. The mean log levels of miR-449 expression in tumor and adjacent non-tumor tissues are -1.14 and -2.65, respectively (p=0.02); for miR-let-7g, the mean log levels of tumor and adjacent non-tumor expression are 5.40 and 5.49 respectively (p=0.87). The relationship between exposure to chemical carcinogens as indicated by levels of polycyclic aromatic hydrocarbon (PAH)-DNA adducts and miR expression was also investigated. The mean log levels of miR449 in tumor tissues with high, moderate and low PAH-DNA adduct levels are -2.27, -2.22 and -0.43, respectively (p=0.02). The log levels of miR449 in tumors with and without cirrhosis are 0.02 and -1.42, respectively (p=0.02). These findings suggest that chemical carcinogen exposure and cirrhosis status may affect miR449 expression in HCC. Larger sample sizes and studies on the underlying mechanisms of miR449 and mir-let-7g expression in HCC are needed. Citation Format: Yu-Jing Zhang, Hui-Chen Wu, Jing Shen, Ming-Whei Yu, Regina M. Santella. Detection of mir-449 and mir-let-7g expression in Taiwan paired hepatocellular carcinoma. [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 4177. doi:10.1158/1538-7445.AM2013-4177