**7. Conclusion**

Disruption of GJIC is closed associated to hepatocarcinogenesis process despite of hepatocarcinoma cells rarely present mutation in connexin genes. Epigenetic events can be involved with to lose functional GJ. Change in connexin expression profile (from Cx32 to Cx43) is frequently observed in liver tumor cells. Abnormal localization of connexin (cytoplasmatic instead plasma membrane) also is characteristic de tumor cells. Thus, many studies were employed in the past to verify if connexin could be target of therapeutic approaches. The studies about connexin biosynthesis, traffic, docking at plasma membrane and degradation were very important to understand as functional channels are formed as well as the possible protein partners related with delivery and removal of connexin at plasma membrane. The phosphorylation status of connexin is very critical in relation this issue, likewise the participation of many proteins (signaling pathways, cytoskeleton and cell-to-cell adhesion). The attention for connexins was reinforced when it was observed that functional GJIC was restored in tumor cells by forced expression of connexin. Fortunately along of time a lot of information were collected and today we know that connexins exert tumor suppressor activity on hepatocarcinoma cells dependent and independent-functional GJIC. So, in the future it is possible that connexin will be used as therapeutic target for hepatocarcinoma.
