Fig. 7

UTMD inhibited autophagy in a PGRMC1-dependent manner in IR-treated glioblastoma cells. a, b GL261 and U251 cells were pretreated with AG-205 (10 μmol/L) for 1 h and then cells were treated with UTMD followed by IR (2 Gy) exposure. After 24 h, cells were collected and lysed, then Western blotting analysis was performed. The bar graphs show the quantification of the indicated proteins. GL261 and U251 cells were transfected with lentiviral vectors encoding PGRMC1 or PGRMC1 siRNA. Then, the cells were treated with UTMD followed by IR (2 Gy) exposure. c–f The expression of LC3B2, p62, PGRMC1 and ACTB was detected by Western blotting. The bar graph shows the quantification of the indicated proteins. Values are expressed as mean ± SD (n = 3). *P < 0.05, **P < 0.01 vs. the vehicle-treated control group; ^#P < 0.05 vs. IR group; ^&P < 0.05, ^&&P < 0.01 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, LC3B light chain 3 beta, p62 sequestosome 1, ACTB β-actin, PGRMC1 progesterone receptor membrane component 1, SD standard deviation, a.u. arbitrary units