ndant surface expression of DHCR24 has only been observed in HCC cells . Before surface DHCR24 can be used in clinical applications as a specific target in HCC, it is necessary to verify the surface expression of DHCR24 in primary hepatic cells and liver tissue derived from HCC and to compare the surface expression levels of DHCR24 in HCC cells, normal hepatocytes, and other types of cancer cells. In HB-derived HepG2 cells, surface expression of DHCR24 was slightly induced by 2-152a MAb treatment. Therefore, in some types of cancer cells, surface expression of DHCR24 might be induced by certain stimuli. The molecular mechanism underlying the constitutive surface expression of DHCR24 in HCC cells is not yet known. Therefore, we should elucidate the entire mechanism before applying surface DHCR24 for clinical use as a therapeutic target against HCC. HCC does not respond to most chemotherapeutic drugs, so there is an urgent need to develop new drugs with different mechanism of action. Targeted therapy using MAb represents a novel promising strategy. Actually, some clinical trials of antibody therapies for advanced HCC are in progress. Recently, novel HCC-specific target molecules such as Glypican3, EGFR variant III, granulin-epithelin precursor and AF-20 antigen were discovered and attempts to treat HCC by using the therapeutic antibody targeting these molecules are underway. There are mainly two patterns on the usage of the targeting antibody. One usage is to utilize the effector function of the antibody and antagonistic action that inhibit proliferative signaling pathway in cancer. Anti-GPC3 MAb and anti-EGFRvIII MAb show antitumor activity mediated through ADCC and/or CDC. In addition, anti-EGFRvIII MAb, anti-GEP MAb and VH domain antibody derived from anti-GPC3 MAb inhibit EGFR signaling, GEP signaling and Hippo signaling, respectively, which are strongly activated in HCC. Additively, these therapeutic antibodies could sensitize HCC to the chemotherapeutic agents. Another usage is to utilize the antibody as delivery tool for cancer and incorporate the cytotoxic payload to cancer cells MedChemExpress 2883-98-9 pubmed ID:http://www.ncbi.nlm.nih.gov/pubmed/19768415 mediated through the bound antibody. Binding of AF-20 MAb to AF-20 antigen on the cell surface of HCC triggers rapid internalization at 37C. Based on this property, targeting approaches for HCC such as the transfer of suicide genes and incorporation of chemotherapeutic agents are devised by using AF-20 MAb. 2-152a MAb could fulfill these both usages, therefore, can be a promising therapeutic antibody against HCC. ~~ Contact inhibition of cell movement and proliferation is essential for proper morphogenesis and maintenance of tissue architecture during embryonic development and regeneration in adults. Deregulation of contact inhibition is thought to play a role in tumorigenesis. Contact inhibition is a phenomenon that can be observed between two moving and proliferating cells in culture. When the cells collide, they gradually reduce movement and proliferation, and eventually stop moving and proliferating. To understand the molecular mechanisms underlying the contact inhibition, the molecular mechanisms for cell–cell adhesion, cell movement, cell proliferation, and mutual interactions among these PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19768759 three cellular responses have 1 / 20 Regulation of Contact Inhibition by Necl-4 funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competi