Objective:To investigate the effect of long non-coding (lnc) RNA HCP5 on the radiation sensitivity of glioma cells and underlying mechanism.Methods:The glioma cells U251 and U87 were irradiated with 0, 2, 4, 6, and 8 Gy rays as different doses.si-Con, si-HCP5, pcDNA, and pcDNA-HCP5 were transfected into cells U251 and U87, recorded as si-con group, si-HCP5 group, pcDNA group, and pcDNA-HCP5 group.si-Con and si-HCP5 were transfected into cells U251 and U87, and then irradiated with 4 Gy rays, respectively, recorded as IR+ si-con group and IR+ si-HCP5 group, the cells only irradiated with 4 Gy rays were recorded as IR group.After si-HCP5 with anti-miR-con and anti-miR-508-3p was co-transfected into cell U251 and U87, respectively, irradiated with 4 Gy rays, recorded as IR+ si-HCP5+ anti-miR-con group and IR+ si-HCP5+ anti-miR-508-3p group, respectively, the transfection was performed by liposome method.RT-qPCR was used to detect the expression of miR-508-3p and HCP5.Cell clone formation assay was used to detect the radiosensitivity of glioma cells.Flow cytometry was used to detect apoptosis, dual luciferase Reporter gene detection experiments detects fluorescence activity.Results:HCP5 was highly expressed in radiation-treated glioma cells, and miR-508-3p was lowly expressed.After silenced HCP5, U251 and U87 cells had enhanced radiosensitivity and apoptotic rate((16.67±1.68) vs (3.58±0.62), t=21.929, P<0.05; (12.32±1.08) vs (4.48±0.71), t=18.198, P<0.05) was increased, and γ-H2AX( (0.45±0.04) vs (0.23±0.05), t=10.307, P<0.05; (0.38±0.04) vs (0.24±0.03), t=8.400, P<0.05), Cleaved caspase-3((0.37±0.04) vs (0.16±0.03), t=12.600, P<0.05; (0.38±0.04) vs (0.22±0.03), t=9.600, P<0.05) expressions were increased.Compared with silencing HCP5 or radiation treatment alone, silencing HCP5 and radiation treatment of U251 cells simultaneously, the apoptosis rate ((25.34±1.54) vs (16.67±1.68), t=11.413, P<0.05; (25.34±1.54) vs (11.13±1.06), t=22.802, P<0.05) was significantly increased, and γ-H2AX((0.69±0.05) vs (0.45±0.04), t=11.245, P<0.05; (0.69±0.05) vs (0.31±0.04), t=17.804, P<0.05), Cleaved caspase-3 ((0.52±0.06/0.37±0.04, t=6.240, P<0.05) (0.52±0.06/0.34±0.04, t=7.488, P<0.05) expressions were increased.The expressions of p-PI3K ((0.21±0.02) vs (0.52±0.04), t=20.795, P<0.05; (0.26±0.23 ), ( 0.67±0.07), t=5.116, P<0.05), p- AKT ((0.22±0.03) vs (0.66±0.07), t=17.332, P<0.05; (0.23±0.04) vs (0.71±0.03), t=28.800, P<0.05) in U251 and U87 cells were decreased.HCP5 can target the regulation of miR-508-3p expression; interfering with miR-508-3p reversed the effects of silent HCP5 and radiation on the radiation sensitization and apoptosis of U251 and U87 cells.It reduced the expression levels of reducing γ-H2AX and Cleaved caspase-3, while increased the expression levels of p-PI3K and p-AKT. Conclusion:Silencing lncRNA HCP5 can enhance the radiation sensitivity of glioma cells and promote apoptosis.The mechanism may be related with the miR-508-3p and PI3K/Akt signaling pathway, which will provide new targets and new ideas for glioma treatment.

Objective: To investigate the effect of lncRNA GIHCG on the radiosensitivity of glioma cells and its mechanism. Methods: The expression levels of GIHCG and miR-146a-3p in human brain normal glial cells HEB and glioma cell lines U251, A172, SHG139 and U87 were quantitatively measured by qRT-PCR assay. U251 and SHG139 cells were used for subsequent experiment. After silencing the expression of GIHCG or overexpressing miR-146a-3p in U251 and SHG139 cells, cell proliferation was detected by MTT assay, cell apoptosis was detected by flow cytometry, cell radiosensitivity was detected by colony formation assay and the expression levels of CDK1, CyclinD1, Bcl-2 and Bax proteins were measured by Western blot. The bioinformatics software predicted the presence of a binding site for GIHCG and miR-146a-3p. Dual luciferase reporter gene assay and qRT-PCR assay were adopted to verify the targeting relationship between GIHCG and miR-146a-3p. Results: Compared with HEB cells, the expression of GIHCG was significantly up-regulated in glioma U87, U251, A172 and SHG139 cells (all P<0.05), whereas that of miR-146a-3p was remarkably down-regulated (P<0.05). Silencing GIHCG expression or overexpression of miR-146a-3p significantly decreased the U251 and SHG139 cell survival rate, survival fraction and the expression of CDK1, CyclinD1 and Bcl-2 proteins (all P<0.05), whereas considerably increased the apoptotic rate and expression of Bax protein (both P<0.05). GIHCG performed targeted negative regulation of miR-146a-3p expression in U251 and SHG139 cells and inhibition of miR-146a-3p expression reversed the effect of silencing GIHCG on proliferation, apoptosis and radiosensitivity of glioma cells. Conclusion Silencing GIHCG expression up-regulates the expression of miR-146a-3p, thereby enhancing the radiosensitivity of glioma cells.