Therefore, an increase in MMP-1 expression MK-0683 promoted by galectin-3 might have dual effects, namely, PAR-1 activation and ECM degradation, and both are critical for gastric cancer metastasis. However, how galectin-3 regulates MMP-1 expression is still unclear, because the expression of MMP-1 is regulated by a series of complex events including crosstalk between several transcriptional factors, such as AP-1, signal transducer and activator of transcription-3, MAP kinase, and hypoxia-inducible factor-1 in hypoxia. Establishing the zebrafish embryo model for studying the migration and invasion of gastric cancer cells is a particular accomplishment of this study because suitable animal models were not available for studying human gastric cancer metastasis until now. The zebrafish model to study genetically engineered cancers and/or tumor xenografts, has many advantages, including feasibility of forward and reverse genetic analyses, transparency of the embryos, and suitability for GFP labeling of vessels. This study showed that RFP labeled gastric cancer cells invaded blood vessels while galectin-3, MMP-1 or PAR-1 silenced gastric cancer cells could not. Thus, the zebrafish embryo seems to be a promising model for studying invasion and metastasis of cancer cells, although further studies are clearly needed to confirm this finding. In conclusion, our studies demonstrated that galectin-3 accelerated gastric cancer cell motility by up-regulating of PAR1 and MMP-1. Further studies are clearly needed to establish the role of galectin-3 in cancer metastasis and its suitability as a therapeutic target for selected cancers. Cardiovascular disease is a leading cause of morbidity and mortality worldwide. Heart failure due to ischemic coronary artery disease is currently the most common cardiac disorder and it correlates with a worse prognosis. The physiological, histological and molecular changes associated with clinical ischemic heart disease have been clarified with the use of experimental models of myocardial infarction developed in both large animals, including dogs and swine, as well as in small rodents. The latter are more applicable for high-throughput screening of novel therapeutic approaches, due to the easy maintenance, short reproductive cycle and to the latest advances in gene-targeting and transgenic technologies. In recent years, the evaluation of cardiac regenerative potential of newly developed therapies, as is the case of gene-delivery and transplantation of stem/progenitor-cells, has been primarily explored in rat and mouse models of surgically-induced myocardial ischemia. The so-called left anterior descending coronary artery ligation is the prominent model in these studies, and the infarct size has been considered a key parameter for assessing the success of the novel therapy. A strong correlation between the infarction size and the functional and hemodynamic alterations following myocardial infarction is generally observed and therefore considered a fundamental measure in the assessment of the morphological and functional consequences of infarction.