LINC01123 potentially correlates with radioresistance in glioma through the miR‐151a/CENPB axis

Radiotherapy represents the most effective nonsurgical therapy, whereas acquired radioresistance remains a major challenge in glioma treatment. Deregulation of long noncoding RNAs (lncRNAs) is frequently involved in tumorigenesis. This study investigates the role of LINC01123 in radioresistance in glioma with molecules involved. LINC01123 was identified as the most upregulated gene in a glioma gene expression dataset GSE103227. LINC01123 was highly expressed in the radioresistant glioma tissues radioresistant glioma U251 (U251R) cells. Downregulation of LINC01123 reduced cell proliferation and colony formation abilities, as well as resistance to apoptosis of the U251R cells after 4 Gy X-ray irradiation. The micro(mi)RNA-151a gene (miR-151a) was a poorly expressed miRNA in glioma, and it was a target of LINC01123. The centromere protein B gene (CENPB) mRNA was a direct target of miR-151a and demonstrated a positive correlation with LINC01123 in glioma tissues and cells. Further inhibition of miR-151a or overexpression of CENPB restored radioresistance of glioma cells. In addition, silencing of LINC01123 suppressed growth of xenograft tumors formed by U251R cells in nude mice. To conclude, the present study demonstrates that LINC01123 serves as a sponge for miR-151a and upregulates CENPB expression to increase the radioresistance of glioma cells in vitro and in vivo.

留言 (0)

沒有登入
gif