Anti-CCND2 monoclonal antibody, clone DZ-E3

Gastric cancer (GC) is still the second lethal malignancy worldwide. Mounting evidence indicates that lncRNAs (long-non coding RNAs) play vital roles in tumorigenesis. But, the role of lncRNAs in GC is still largely unclear. Firstly, QRT-PCR were performed to asses lncRNA CCND2-AS1 expression 64 pairs of gastric cancer tissues (case group) and matched non-tumor tissues (control group). Both loss- and gain-functions assays were conducted by transfection. The cell viability, proliferation and cell cycle status after transfection were assessed by CCK-8 assay, clone formation assay, and FCM. Our results firstly show that LncRNA CCND2-AS1 is upregulated in GC tissues and cell lines. Moreover, CCND2-AS1 can promote GC cell proliferation and growth through Akt signaling. We demonstrate that CCND2-AS1 promoted GC cell growth via affecting Akt signal pathway and which suggest CCND2-AS1 might act as a potential therapeutic target in GC.

Previous studies have shown that microRNA (miR)-610 is crucial in a variety of biological processes in various types of human cancer cells. However, the role of this microRNA in glioblastoma (GBM) is presently unclear. In this study, the role of miR-610 in cell proliferation was investigated in GBM. It was demonstrated that miR-610 expression is markedly downregulated in GBM cells and GBM tissues compared with normal human astrocytes (NHAs) and normal brain tissue, respectively. Ectopic expression of miR-610 reduced the proliferation and anchorage-independent growth of GBM cells, whereas inhibition of miR-610 promoted this effect. Bioinformatics analysis further revealed cyclin D2 (CCND2) and AKT3, putative tumor promoters, as potential targets of miR-610. Data from reporter assays showed that miR-610 directly binds to the 3-untranslated region of CCND2 and AKT3 mRNA, and represses their expression at the transcriptional and translational levels. In conclusion, the data provide compelling evidence that miR-610 functions as an anti-onco-miRNA, which is important in inhibiting cell proliferation in GBM, and its anti-oncogenic effects are mediated chiefly through direct suppression of CCND2 and AKT3 expression.