miR-204 was found to be downregulated in gastric cancer (GC) tissues, and the effect of miR-204 function on gastric cancer remains as a mystery. Therefore, this study was aimed at investigating the potential role of miR-204 involved in GC progression. Tissues collected from 60 gastric cancer patients were selected as the case group, while the matched normal paracancer tissues as controls. miR-204 expression levels in tissues and GC cells were detected using real-time fluorescent quantitative PCR. Luciferase assay was adopted to validate the interaction between potential gene targets and miR-204. Transwell assay was performed to evaluate the metastasis of GC cells. By building the epithelial-mesenchymal transition (EMT) model in vitro through the addition of transforming growth factor beta 1 (TGF-β1), expressions of miR-204 and snai1 in the EMT model together with their respective effects on EMT were evaluated. miR-204 was significantly downregulated in GC tissues and invasive GC cells (P < 0.05). The over-expression of miR-204 or downregulation of snai1 could significantly inhibit the metastasis and invasion of GC cells both in vitro and in vivo. The upregulated miR-204 expression or inhibited snai1 expression could suppress the EMT process in EMT in vitro models. Our study provided evidence that miR-204 may suppress the metastasis and invasion of GC cells through the regulation of the EMT process by targeting snai1.

Pancreatic carcinoma is one of the most malignant and aggressive cancers. Increased motility and invasiveness of pancreatic cancer cells are believed to be associated with epithelial-to-mesenchymal transition (EMT). However, the molecular basis of EMT in pancreatic cancer cells is poorly understood. In this study, we examined the relationship between Jun dimerization protein 2 (JDP2), which is an AP-1 inhibitor, and EMT in human pancreatic carcinoma cells. We demonstrated that transforming growth factor-β1 (TGF-β1) promoted epidermal growth factor (EGF)-induced EMT in co-treated human pancreatic BxPC3 cells and that JDP2 overexpression reversed the EMT that was induced by co-treatment with TGF-β1 and EGF. These results suggest that EGF plays a principal role in EMT through its association with TGF-β1 in human pancreatic BxPC3 cells and that JDP2 may be a molecular target for pancreatic carcinoma intervention.

Genistein and trichostatin A (TSA) are two chemotherapeutic compounds with antitumor effects in different types of cancer cell. However, the effects of genistein and TSA on the HEp-2 laryngeal cancer cell line remain to be fully elucidated. In the present study, it was found that genistein and TSA inhibited cell growth and cell migration, and promoted apoptosis in the HEp-2 laryngeal cancer cell line. The HEp-2 cells were treated with genistein, TSA or the two compounds in combination. Cell proliferation and apoptosis were measured using an MTT assay, Annexin V/propidium iodide staining and a TUNEL assay. Cell invasion was determined using a Matrigel-based Transwell assay. Western blotting was used to examine the activation of the Akt pathway and the expression levels of pro-or anti-apoptotic proteins. Treatment with either genistein or TSA alone mildly inhibited cell viability, growth and invasion, and induced the apoptosis of the laryngeal cancer cells, whereas more marked effects were observed in the cells treated with the combination of the two compounds. In addition, genistein reversed endothelial growth factor-induced epithelial-mesenchymal transition (EMT) in the HEp-2 cells, the effect of which were was further increased by joint application with TSA. Treatment of the HEp-2 cells with genistein and TSA led to a significant reduction in the phosphorylation of Akt and activation of its downstream target, and resulted in peroxisome proliferator-activated receptor-γ cleavage, increased expression of B cell lymphoma-2 (Bcl-2)-associated X protein and reduced the expression of Bcl-2. In conclusion, the present study demonstrated that, with the involvement of TSA, genistein exhibited substantial advantages in inhibiting laryngeal carcinoma cell growth, invasion and EMT, and induced apoptosis, compared with genistein treatment alone, which occurred through the regulation of Akt activation and the apoptotic pathway.