RNaseH2A is involved in human gliomagenesis through the regulation of cell proliferation and apoptosis.

摘要: Mutations in the RNaseH2A gene are involved Aicardi‑Goutieres syndrome, an autosomal recessive neurological dysfunction; however, studies assessing relation to glioma scarce. This study aimed assess role of and unveil underlying mechanisms. was silenced glioblastoma cell lines U87 U251. Gene expression assessed cells transfected with shRNA or scramble by microarrays, validated quantitative real time PCR. Protein evaluated western blot analysis. Cell proliferation MTT assay; cycle distribution apoptosis were analyzed flow cytometry. Finally, effects on colony formation tumorigenicity in vitro a mouse xenograft model, respectively. successively knocked down U251 cells. Notably, silencing resulted impaired proliferation, 70.7 and 57.8% reduction U251 cells, respectively, being blocked G0/G1 phase in vitro. Meanwhile, clone significantly reduced knockdown, which also increased approximately 4.5-fold. In nude mice, tumor size decreased after knockdown: 219.29±246.43 vs. 1160.26±222.61 mm3 for control group; similar findings obtained weight (0.261±0.245 1.127±0.232 g) groups, respectively). microarray data, shown modulate several signaling pathways responsible apoptosis, such as IL-6 FAS pathways. may be human gliomagenesis, likely regulating apoptosis.