Objective:To explore the potential mechanisms of lymphatic metastasis of GC cells regulated by ring finger protein (RNF180).Methods:Associations between clinicopathologic, survival data, and RNF180 expression in GC tissues were analyzed. The effects of RNF180 re-expression and genome microarraywere determined in growth, proliferation, invasion, and lymphangiogenesis assays.Results:RNF180 was silenced or down-regulated in 76.1%of GC tissues compared with 41.8% of paired non-tumor tissues. RNF180 protein expression in GC tissues was negatively related to the number of metastatic lymph nodes. RNF180 was down-regulated in 100% (7 of 7) of GC cell lines. Re-expression of RNF180 in HGC-27 GC cells reduced colony formation, proliferation, migration and invasion in vitro, and tumor growth and tumor lymphangiogenesis in mice it also down-regulated HGF, MMP-2, MMP-14, VEGF-C/D and CCR-7 in vitro, and Podoplanin in tumor tissue of mice.Conclusion:RNF180 is a suppressor gene involved inthe several biological events of GC cell including the proliferation, invasion, and tumor lymphangiogenesis.

AIM： To investigate the efficiency of cytosine deaminase adenoviral/5-fluorocytosine system on prostate cancer cell lines. METHODS: Cell culture, infectivity test and sensitivity test, observing the bystander effect and animal model experiment were carried out. RESULTS: All the established prostate cancer cell lines were eventually infectable, but ratio of vector/cell and time of exposed at which infection occurs was dependent on the cell lines. The expression of transfered cytosine deaminase gene peaked at different days, but persisted beyond 11 days. The prostate cell lines were sensitized to the 5-fluorocytosine by infection with the cytosine deaminase gene adenoviral vector, and only 5% of the LNCap and 10% of the RM-1 cells infected were required for 100% cell death. In the animal model, there was significant eradiation of tumor growth at the ratio of 400 vector particles/cell and with the systematic treatment of 5-fluorocytosine. CONCLUSION: The adenoviral vector carrying a cytosine deaminase transcription unit can sensitize the prostate cancer cell lines to 5-fluorocytosine, and the system can significantly inhibit the growth of prostatic tumor in mice.

AIM:Increasing evidence suggests that carbohydrate-binding proteins play an essential role in tumor growth and metastasis .Ga-lectin-3, a multifunctional protein of an expanding family of β-galactoside-binding animal lectins , is the major nonintegrin cellular laminin-binding protein , and is implicated in a variety of biologic events , such as inflammation and angiogenesis .Because galectin-3 expression was shown to participate in mediating tumor angiogenesis and initiate signaling cascades in several diseases .We hypothe-sized that galectin-3 may promote pulmonary vascular endothelial neovascularization .METHODS:Hypoxic and MCT rat model of pul-monary artery remodeling was used .The mRNA and protein levels of galectin-3 in rats were measured by in situ hybrization and West-ern blot analysis.Endothelial cell (EC) proliferation, migration and tube formation were measured using MTT , cell scratch and Matri-gel assays, respectively.Protein expression was quantitated by Western blot analysis .LC 3A/B staining was detected with cellular im-munofluorescence staining .RESULTS:We found that galectin-3 was localized on the intima and adventitial wall .Galectin-3 was in-creased after rat hypoxia and MCT administration .Galectin-3 promoted EC proliferation , migration and tube formation , while its roles were reversed by RNA interference.Galectin-3 induced Atg 5, Beclin-1, LAMP-2, and LC 3A/B expression increases.Galectin-3 al-so increased LC 3A/B staining in ECs.Akt/mTOR and GSK-3βsignaling pathways were activated after galectin-3 treated ECs using its specific phosphorylation antibodies , while blocked it with LY294002 inhibited cell autophagy and EC dynamic alterations induced by galectin-3.CONCLUSION:These findings demonstrate that galectin-3 can induce an Akt signaling cascade leading to cell autoph-agy, and then the differentiation and angiogenesis of pulmonary artery endothelial cells .

Revisiting the Seed-and-soil Theory of Cancer Metastasis

In 1889, Paget proposed a "Seed-and-Soil" theory for cancer metastasis.According to this theory, cancer metastasis is not random, and one remote organ is more prone to be the seat of secondary tumor growth than another.