Knockdown of long non-coding RNA PCAT1 in glioma stem cells promotes radiation sensitivity.

This study aimed to investigate the function of glioma stem cells (GSCs) and the role of PCAT1. This study dissociated the differences between GSCs and glioma cells in terms of apoptosis rate and γH2AX positive cells levels after radiation. Microarray was carried out to detect that expressed PCAT1, and it was testified by RT-qPCR. After transfection, GSCs were used to investigate the influence of PCAT1 on radiation sensitivity. Sphere-formation capability was first examined. Cell apoptosis rate after radiation of 0 Gy or 6 Gy was analyzed by flow cytometry, and the level of γH2AX positive cells after 6 Gy radiation were compared. CCK8 assay was used to investigate the cell proliferation and RT-qPCR was used to examine miR-129-5p and HMGB1 expression. GSCs exhibited great capability in sphere formation and lower expression in apoptosis and γH2AX positive cells rates after 6 Gy radiation. PCAT1 had higher expression in GSCs. PCAT1 knockdown restrained the sphere-formation ability, increased the apoptosis rate and DNA damage under the treatment of radiation. Moreover, knockdown of PCAT1 inhibited the cell proliferation. In addition, silencing PCAT1 could increase the expression of miR-129-5p and decrease the expression of HMGB1. PCAT1 was overexpressed in GSCs and played a facilitating role in radiation resistance.