Hepatocellular carcinoma (HCC) is the most common liver cancer and one of the commonest solid malignancies. High mortality rates and poor prognosis of the disease are mainly due to late diagnosis, underlying cirrhosis and resistance to chemotherapy. The risk factors of HCC include infections with hepatitis B and C viruses, along with other conditions that cause cirrhosis like: alcoholism and non-alcoholic steatohepatisis. Wnt/ß catenin signaling pathway plays a vital role in regulating the cell fate during embryogenesis and cell proliferation in adult tissues. In the absence of the Wnt ligand, beta-catenin is phosphorylated through interaction with GSK-3b, APC, axin and subsequently degraded by the ubiquitin-proteasome system. However, when the Wnt ligand binds to the receptor complex of the pathway, the destruction complex is inactivated leading to the accumulation of beta-catenin in the cytoplasm and its translocation to the nucleus where it forms complexes with TCF/LEF family that causes transcriptional activation of target genes. Recent studies suggest that cancer stem cells play a key role in liver carcinogenesis. Mutations in beta-catenin and activation of Wnt/ß-catenin signaling pathway is likely to cause abnormal proliferation and enhanced self-renewal of hepatic progenitor cells resulting in their transformation into cancer stem cells. Thus understanding the characteristics and function of liver cancer stem cells and their response to beta-catenin inhibitors is crucial to the development of novel, more effective drugs and improving patient survival. In this study we have used various drugs to target Wnt/beta-catenin signaling pathway in hepatic carcinoma cell lines. We assessed the effect of the inhibitors of beta-catenin on the expression of stem cell markers in these cell lines and will present the results of the study.


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