Smac is a novel pro-apoptotic protein. To explore the effect of apoptosis of human colorectal carcinoma Caco-2 cells and the expression of Smac protein induced by norcantharidin, for providing reliable evidence for clinical application. Methods: Caco-2 cells of human colorectal carcinoma were cultured by cell culture technipue. Cellular proliferation activeties were assayed by MTT. The

apoptosis of cells was assayed by flow cytometry. The expression of Smac protein was detected by Western blot after stimulation by norcantharidin. Results: NCTD inhibited the growth and proliferation of Caco-2 cells in a dose and time dependent manner, with an IC50 value of 59.37 μg/ml at 36 h. The apoptosis rates of Caco-2 cells after stimulation by norcantharidin

C646 were higher than control groups (P < 0.01). The expression of Smac protein increased from 0.147 ± 0.028 to 0.726 ± 0.060 3-deazaneplanocin A at 36 h after NCTD treated cells (P < 0.01). Conclusion: This study shows the inhibition of NCTD on Caco-2 cells. The expression of Smac protein increased after NCTD treated cells. The mechamism of NCTD antitumor may be related to Smac, the key factor of cell apoptosis signaling pathway. Key Word(s): 1. Norcantharidin; 2. Colorectal carcinoma; 3. Livin; 4. Caspase-3; Presenting Author: NANA TANG Additional Authors: HUARUI SHI, JIEHONG ZHANG Corresponding Author: NANA TANG Affiliations: Jiangsu Province Hospital; the First Affiliated Hospital of Nanjing Medical University Objective: Vasculogenic mimicry (VM) describes the unique ability of highly aggressive tumor cells to express endothelial cell-associated genes (such as EphA2 and VE-cad) and form ECM-rich, patterned tubular networks when cultured on a three-dimensional matrix. However, the exact mechanism underlying click here of VM still needs to be unraveled. This study contributes new observations demonstrating that hypoxia inducible factor-1alpha (HIF-1α) can increase the expression of EphA2 and LN5γ2

by up-regulating VE-cadherin expression in esophageal cancer cells during formation of VM. Methods: Two esophageal cancer cell lines Eca109 and TE13 were transfected by plasmid harboring small interfering RNA targeting for HIF-1α or VE-cadherin. The formation of tubular networks of Eca109 and TE13 cells was analyzed by three-dimensional culture in vitro. The relationship of the expression of HIF-1α and VE-cadherin, EphA2, LN5γ2 was measured by western blot and Realtime PCR. Results: Both Eca109 and TE13 formed typical tubular networks. The number of tubular networks remarkably decreased when HIF-1α or VE-cadherin was knocked down. The expressions of VE-cadherin, EphA2 and LN5γ2 were dramatically inhibited in HIF-1α-silencing cells. When VE-cadherin was knocked down, EphA2 and LN5γ2 expression decreased, while HIF-1α expression had no change.