ABSTRACT
Epithelial-mesenchymal transition (EMT) is a crucial step in tumor progression and has an important role during cancer invasion and metastasis. The proteins of the inhibitor of growth (ING) candidate tumor suppressor family are involved in multiple cellular functions such as cell cycle regulation and apoptosis. ING5 is a member of the family. However, the role of ING5 in breast cancer is still unclear. Thus, the aim of this study is to explore the role of ING5 in breast cancer. In the present study, we showed that ING5 is involved in the pathogenesis of breast cancer. ING5 is down-regulated in breast cancer tissues and cell lines. Overexpression of ING5 significantly inhibited breast cancer cell migration, invasion, and EMT phenotype, moreover, overexpression of ING5 significantly the phosphorylation of PI3K and Aktin in breast cancer cells. In conclusion, our findings show that ING5 can efficiently inhibit the EMT progression in breast cancer cells by suppressing PI3K/Akt signaling pathway. Therefore, ING5 may be a good molecular target for the prevention and treatment of breast cancer.
ABSTRACT
BACKGROUND/AIMS: : This study aims to comparing the gene expression profiles and molecular interactions among gastric cardiac adenocarcinomas (GCA), gastric noncardiac adenocarcinomas (GNCA) and their adjacent normal tissues. METHODOLOGY: Gene expression profile of GSE29272 was downloaded from Gene expression omnibus. Differentially expressed genes (DEGs) were identified at the cut-off of p-value ≤ 0.01. Gene ontology (GO) enrichment analysis was further performed for the DEGs, and then the binding sites of the transcriptional factors and the specific protein-protein interactions were analyzed. RESULTS: Total 1024 DEGs were screened, including 741 up-regulated genes and 283 down-regulated genes. VSNL1 (visinin-like protein-1) is expressed relatively higher in the GNCA and could be its molecular biomarker, as KRT14 (cytokeratin 14) in the GCA. GO analysis showed that the analogous cancer-relevant factors network appears in these two cancer subgroups. The DEGs in the GCA tend to be bound by SPIB and ZNF354C. FN1 lies in the center of the protein-protein interaction networks of the two cancer subgroups. CONCLUSIONS: We found out the RNA expression level of the two gastric cancers varied greatly from the normal tissues while gene expression profile of them were very similar, however, the different biomarker and transcriptional factors indicate the differences of two mechanisms.
