Contents I. Introduction
Hepatocellullar carcinoma (HCC) represents the main form of liver cancer [1] which is ranked as the third most common cause of cancer death [2] [3]. The identified carcinogens of HCC include hepatitis B virus (HBV) hepatitis C virus (HCV) alcohol, tobacco and aflatoxin [4] [5]. Many cellular pathways leading to the tumorigenesis of HCC have been identified. One of such critical pathways is apoptosis, which is a mechanism of programmed cell death that has an implication in the tumor growth [9]. In normal cells, apoptosis helps maintain the normal cell number. However, inhibition of apoptosis that is usually found in the tumor cells always leads to the uncontrolled proliferation of tumor cells, which in turn contributes to apparent increase in tumor size and metastasis. Cytokines, which are growth factors that control cell proliferation and differentiation, have been reported to play a major role in apoptosis pathway in HCC [6] [7]. Other genetic regulatory mechanisms have also been reported to implicate in HCC. Tak1 gene has been reported to suppress a procarcinogenic pathway in HCC [8]. Sustained expression of HGFK1 gene has been discovered to inhibit tumor angiogenesis [10]. Besides, gene therapy has also become common in cancer treatment. One such example of gene therapy in HCC patients is an approach that targets p53 gene [11].
