JMJD5'in karaciğer kanserindeki rolü

Being one of the most common cancer types in human population, hepatocellular carcinoma (HCC) has high rate of deaths due to the challenges in its diagnosis and treatment. In recent years, epigenetic regulators have come into play in HCC research to overcome with those challenges. As potential drug targets, histone demethylases has drawn a lot of interest. In this respect, several studies have focused on a specific member of this family, JMJD5, suggesting its possible function in tumor suppression, while the opposite argument has also been proposed by several reports. Preceding studies on JMJD5 in our lab also pointed to a possible tumor suppressor function. Hence, this study aimed to elucidate the role of JMJD5 in liver cancer development using SNU449 HCC cell line stably expressing JMJD5. For this purpose, stable clones overexpressing wild-type and mutant JMJD5 as well as controls were generated. A comparative analysis of these clones was performed. No definite results could be obtained for the effect of JMJD5 on cell proliferation, but the number of cells in G1 declined, whereas that in G2/M inclined in clones expressing wild-type and mutant JMJD5, suggesting that JMJD5 affects cell cycle progression. In addition, cell motility was decreased, while anchorage-independent colony formation ability was enhanced in both mutant and wild type JMJD5-expressing clones. Decrease in cell motility is considered to be anti-tumoral, whereas anchorage-independent growth is a malignant change. Our findings suggest that JMJD5 may have a quite complex role in liver tumorigenesis. Further in vivo studies may help to clarify some of these apparently conflicting in vitro effects.