Panoply™ Human RRM2 Over-expressing Stable Cell Line

The pathogenesis of glioblastoma is associated with multiple processes influenced by dozens of regulatory factors, but the underlying mechanisms regulating glioblastoma progression remain unclear. Here, researchers investigated how ribonucleotide reductase M2 subunit (RRM2) affects the proliferation, invasion, migration, and apoptosis of human glioblastoma cells. Silencing RRM2 inhibited glioblastoma cell proliferation, invasion, and migration, while increasing apoptosis. Overexpression of RRM2 promoted cell proliferation, migration, and invasion, but inhibited apoptosis. In in vivo experiments, overexpression of RRM2 accelerated tumor growth of glioblastoma cells. These studies indicate that RRM2 is highly expressed in human glioblastoma cells. RRM2 promotes the proliferation, migration, and invasion of human glioblastoma cells, but inhibits apoptosis.

The cell viability of RRM2 knockdown cells was significantly weaker than that of the control and NC groups, while the cell viability of RRM2 overexpressing cells was stronger than that of the control and NC groups (Figure 1a). The colony formation assay showed no significant difference between the control and NC groups. However, the number of colonies decreased in the RRM2 knockdown group, while it increased in the RRM2 overexpression group (Figure 1b and 1c). Immunofluorescence staining results showed that the red fluorescence representing PCNA protein was significantly weaker in the RRM2 knockdown group than in the RRM2 overexpression group. PCNA can be used as an indicator of cell proliferation status. Furthermore, there was no significant difference between the control and NC groups (Figure 1d). These results indicate that the RRM2 gene promotes the proliferation of glioblastoma cells.

Figure 1. RRM2 promoted proliferation of glioblastoma cells. (Li C, et al., 2018)