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    UTMD-induced autophagosome accumulation in IR-exposed glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s. Then, the cells were exposed to IR (2 Gy), and 24 h later, the level of LC3B2 was detected by Western blotting analysis and the indicated protein was quantified. c GL261 cells were transfected with a plasmid expressing GFP-LC3B. After 24 h, the cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Following fixation, the cells were immediately visualized by confocal microscopy, and the number of GFP-LC3B dots in each cell was counted. d GL261 cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for another 24 h. Autophagosomes were detected by transmission electron microscopy. Arrows indicate the autophagosomes. Values are expressed as the mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, LC3B light chain 3 <t>beta,</t> ACTB β-actin, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units
    Scion Image Release Beta 4.02 Software, supplied by scion corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/-release+beta+4%2E02+software/scion+image+software/pmc08842919-111-18-22
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    scion image-release beta 4.02 software - by Bioz Stars, 2026-10
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    1) Product Images from "Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo"

    Article Title: Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo

    Journal: Military Medical Research

    doi: 10.1186/s40779-022-00369-0

    UTMD-induced autophagosome accumulation in IR-exposed glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s. Then, the cells were exposed to IR (2 Gy), and 24 h later, the level of LC3B2 was detected by Western blotting analysis and the indicated protein was quantified. c GL261 cells were transfected with a plasmid expressing GFP-LC3B. After 24 h, the cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Following fixation, the cells were immediately visualized by confocal microscopy, and the number of GFP-LC3B dots in each cell was counted. d GL261 cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for another 24 h. Autophagosomes were detected by transmission electron microscopy. Arrows indicate the autophagosomes. Values are expressed as the mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, LC3B light chain 3 beta, ACTB β-actin, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units
    Figure Legend Snippet: UTMD-induced autophagosome accumulation in IR-exposed glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s. Then, the cells were exposed to IR (2 Gy), and 24 h later, the level of LC3B2 was detected by Western blotting analysis and the indicated protein was quantified. c GL261 cells were transfected with a plasmid expressing GFP-LC3B. After 24 h, the cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Following fixation, the cells were immediately visualized by confocal microscopy, and the number of GFP-LC3B dots in each cell was counted. d GL261 cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for another 24 h. Autophagosomes were detected by transmission electron microscopy. Arrows indicate the autophagosomes. Values are expressed as the mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, LC3B light chain 3 beta, ACTB β-actin, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Techniques Used: Western Blot, Transfection, Plasmid Preparation, Expressing, Incubation, Confocal Microscopy, Transmission Assay, Electron Microscopy, Standard Deviation

    UTMD inhibited autophagic flux in IR-treated glioblastoma cells. a , b Representative immunoblot and quantification analysis of p62 after GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s followed by IR (2 Gy) exposure. ACTB was used as an internal standard for protein loading. c , d GL261 and U251 cells were pretreated with RAPA (20 nmol/L) or BafA1 (10 nmol/L) for 1 h and then cells were treated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. Total cell lysates were immunoblotted with anti-p62, anti-LC3B, and anti-ACTB antibodies and the bar graphs show the quantification of LC3B2 and p62. e–h GL261 and U251 cells were transfected with lentiviral vectors encoding ATG5 or ATG5 siRNA . Then, the cells were treated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. The expression of LC3B2, p62 and ATG5 was detected by Western blotting. The bar graphs show the quantification of LC3B2, p62 and ATG5. i , j GL261 and U251 cells were pretreated with 3-MA (5 mmol/L) for 1 h and then exposed to UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. Total cell lysates were immunoblotted with anti-p62, anti-LC3B, and anti-ACTB antibodies. The bar graphs show the quantification of LC3B2 and p62. Values are expressed as the mean ± SD ( n = 3). * P < 0.05, ** P < 0.01 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group; & P < 0.05, && P < 0.05 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, ACTB β-actin, LC3B light chain 3 beta, p62 sequestosome 1, RAPA rapamycin, BafA1 bafilomycin A1, 3-MA 3-methyladenine, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units
    Figure Legend Snippet: UTMD inhibited autophagic flux in IR-treated glioblastoma cells. a , b Representative immunoblot and quantification analysis of p62 after GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s followed by IR (2 Gy) exposure. ACTB was used as an internal standard for protein loading. c , d GL261 and U251 cells were pretreated with RAPA (20 nmol/L) or BafA1 (10 nmol/L) for 1 h and then cells were treated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. Total cell lysates were immunoblotted with anti-p62, anti-LC3B, and anti-ACTB antibodies and the bar graphs show the quantification of LC3B2 and p62. e–h GL261 and U251 cells were transfected with lentiviral vectors encoding ATG5 or ATG5 siRNA . Then, the cells were treated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. The expression of LC3B2, p62 and ATG5 was detected by Western blotting. The bar graphs show the quantification of LC3B2, p62 and ATG5. i , j GL261 and U251 cells were pretreated with 3-MA (5 mmol/L) for 1 h and then exposed to UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. Total cell lysates were immunoblotted with anti-p62, anti-LC3B, and anti-ACTB antibodies. The bar graphs show the quantification of LC3B2 and p62. Values are expressed as the mean ± SD ( n = 3). * P < 0.05, ** P < 0.01 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group; & P < 0.05, && P < 0.05 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, ACTB β-actin, LC3B light chain 3 beta, p62 sequestosome 1, RAPA rapamycin, BafA1 bafilomycin A1, 3-MA 3-methyladenine, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Techniques Used: Western Blot, Transfection, Expressing, Standard Deviation

    UTMD inhibited autophagosome fusion with lysosomes in IR-treated glioblastoma cells. GL261 cells were transfected with RFP-GFP-LC3B for 24 h and then exposed to UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. a Representative images of fluorescent LC3 puncta are shown. b Mean numbers of GFP and RFP dots/cell (top). Mean number of autophagosomes (yellow dots in merged images) and autolysosomes (red dots in merged images)/cell (bottom). Values are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group. GFP green fluorescent protein, RFP red fluorescent protein, LC3B light chain 3 beta, IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, MBs microbubbles, SD standard deviation
    Figure Legend Snippet: UTMD inhibited autophagosome fusion with lysosomes in IR-treated glioblastoma cells. GL261 cells were transfected with RFP-GFP-LC3B for 24 h and then exposed to UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. a Representative images of fluorescent LC3 puncta are shown. b Mean numbers of GFP and RFP dots/cell (top). Mean number of autophagosomes (yellow dots in merged images) and autolysosomes (red dots in merged images)/cell (bottom). Values are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group. GFP green fluorescent protein, RFP red fluorescent protein, LC3B light chain 3 beta, IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, MBs microbubbles, SD standard deviation

    Techniques Used: Transfection, Standard Deviation

    UTMD inhibited PGRMC1 expression and binding with LC3B in IR-treated glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs), and then the cells were exposed to IR (2 Gy). PGRMC1 expression was measured by Western blotting. c GL261 and U251 cells were pretreated with UTMD. Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Immunofluorescence staining analysis of PGRMC1 (green) and LC3B (red) expression, the nuclei were stained with DAPI (blue). Values are expressed as mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, ACTB β-actin, LC3B light chain 3 beta, MBs microbubbles, SD standard deviation, a.u. arbitrary units
    Figure Legend Snippet: UTMD inhibited PGRMC1 expression and binding with LC3B in IR-treated glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs), and then the cells were exposed to IR (2 Gy). PGRMC1 expression was measured by Western blotting. c GL261 and U251 cells were pretreated with UTMD. Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Immunofluorescence staining analysis of PGRMC1 (green) and LC3B (red) expression, the nuclei were stained with DAPI (blue). Values are expressed as mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, ACTB β-actin, LC3B light chain 3 beta, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Techniques Used: Expressing, Binding Assay, Western Blot, Incubation, Immunofluorescence, Staining, Standard Deviation

    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
    Figure Legend Snippet: 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

    Techniques Used: Western Blot, Transfection, Expressing, Standard Deviation

    UTMD enhanced the radiosensitivity of glioblastoma via inhibiting PGRMC1-mediated autophagy in mice. Six-week-old female C57BL/6J mice were inoculated in the right caudate putamen with GL261 cells (1 × 10 5 cells per mouse) with or without shPGRMC1-expressing vector to establish the orthotopic glioblastoma mouse model. Seven days after transplantation, the tumor size was evaluated by in vivo bioluminescent imaging. Then, the animals were randomly allocated to treatment groups to receive control treatment or IR (every day, 2 Gy/fraction, 5 fractions) combined with or without UTMD (every other day) treatment over a period of 5 d. On day 20 after tumor transplantation, US and bioluminescent imaging were used to determine the tumor size. Meanwhile, mice were euthanized, and brain tumors were collected. In vivo bioluminescent images (a) and quantification of orthotopic glioblastoma tumors (b) in the brains of mice. c Kaplan–Meier survival analysis of orthotopic glioblastoma-bearing mice. d Orthotopic glioblastoma tumor size was determined by US. White circles indicate tumors. e Immunofluorescent staining and the quantification of Ki67 (green) in orthotopic glioblastoma tumors in the brains of mice. f Tumor tissues were harvested on day 20 after tumor implantation and lysed, and Western blotting analysis was performed. The expression of LC3B2, p62, and PGRMC1 were measured. g The bar graphs showed the quantification of LC3B2, p62, and PGRMC1. Values are expressed as mean ± SD ( n = 6). * P < 0.05 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group; & P < 0.05 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, LC3B light chain 3 beta, p62 sequestosome 1, ACTB β-actin, SD standard deviation, p/s/cm 2 /sr photon per second per square centimetre per steradian, a.u. arbitrary units
    Figure Legend Snippet: UTMD enhanced the radiosensitivity of glioblastoma via inhibiting PGRMC1-mediated autophagy in mice. Six-week-old female C57BL/6J mice were inoculated in the right caudate putamen with GL261 cells (1 × 10 5 cells per mouse) with or without shPGRMC1-expressing vector to establish the orthotopic glioblastoma mouse model. Seven days after transplantation, the tumor size was evaluated by in vivo bioluminescent imaging. Then, the animals were randomly allocated to treatment groups to receive control treatment or IR (every day, 2 Gy/fraction, 5 fractions) combined with or without UTMD (every other day) treatment over a period of 5 d. On day 20 after tumor transplantation, US and bioluminescent imaging were used to determine the tumor size. Meanwhile, mice were euthanized, and brain tumors were collected. In vivo bioluminescent images (a) and quantification of orthotopic glioblastoma tumors (b) in the brains of mice. c Kaplan–Meier survival analysis of orthotopic glioblastoma-bearing mice. d Orthotopic glioblastoma tumor size was determined by US. White circles indicate tumors. e Immunofluorescent staining and the quantification of Ki67 (green) in orthotopic glioblastoma tumors in the brains of mice. f Tumor tissues were harvested on day 20 after tumor implantation and lysed, and Western blotting analysis was performed. The expression of LC3B2, p62, and PGRMC1 were measured. g The bar graphs showed the quantification of LC3B2, p62, and PGRMC1. Values are expressed as mean ± SD ( n = 6). * P < 0.05 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group; & P < 0.05 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, LC3B light chain 3 beta, p62 sequestosome 1, ACTB β-actin, SD standard deviation, p/s/cm 2 /sr photon per second per square centimetre per steradian, a.u. arbitrary units

    Techniques Used: Expressing, Plasmid Preparation, Transplantation Assay, In Vivo, Imaging, Staining, Tumor Implantation, Western Blot, Standard Deviation

    UTMD enhanced the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy. UTMD improved the response of glioblastoma cells to IR via the proposed signaling pathways: UTMD downregulates PGRMC1 expression, thereby inhibiting the combination of PGRMC1 with LC3B2, which is followed by a decrease of autophagosome-lysosome fusion, subsequently disrupting autophagic degradation and ultimately enhancing the radiosensitivity of glioblastoma. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, LC3B light chain 3 beta
    Figure Legend Snippet: UTMD enhanced the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy. UTMD improved the response of glioblastoma cells to IR via the proposed signaling pathways: UTMD downregulates PGRMC1 expression, thereby inhibiting the combination of PGRMC1 with LC3B2, which is followed by a decrease of autophagosome-lysosome fusion, subsequently disrupting autophagic degradation and ultimately enhancing the radiosensitivity of glioblastoma. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, LC3B light chain 3 beta

    Techniques Used: Expressing

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    UTMD-induced autophagosome accumulation in IR-exposed glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s. Then, the cells were exposed to IR (2 Gy), and 24 h later, the level of LC3B2 was detected by Western blotting analysis and the indicated protein was quantified. c GL261 cells were transfected with a plasmid expressing GFP-LC3B. After 24 h, the cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Following fixation, the cells were immediately visualized by confocal microscopy, and the number of GFP-LC3B dots in each cell was counted. d GL261 cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for another 24 h. Autophagosomes were detected by transmission electron microscopy. Arrows indicate the autophagosomes. Values are expressed as the mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, LC3B light chain 3 <t>beta,</t> ACTB β-actin, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units
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    UTMD-induced autophagosome accumulation in IR-exposed glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s. Then, the cells were exposed to IR (2 Gy), and 24 h later, the level of LC3B2 was detected by Western blotting analysis and the indicated protein was quantified. c GL261 cells were transfected with a plasmid expressing GFP-LC3B. After 24 h, the cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Following fixation, the cells were immediately visualized by confocal microscopy, and the number of GFP-LC3B dots in each cell was counted. d GL261 cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for another 24 h. Autophagosomes were detected by transmission electron microscopy. Arrows indicate the autophagosomes. Values are expressed as the mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, LC3B light chain 3 <t>beta,</t> ACTB β-actin, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units
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    UTMD-induced autophagosome accumulation in IR-exposed glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s. Then, the cells were exposed to IR (2 Gy), and 24 h later, the level of LC3B2 was detected by Western blotting analysis and the indicated protein was quantified. c GL261 cells were transfected with a plasmid expressing GFP-LC3B. After 24 h, the cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Following fixation, the cells were immediately visualized by confocal microscopy, and the number of GFP-LC3B dots in each cell was counted. d GL261 cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for another 24 h. Autophagosomes were detected by transmission electron microscopy. Arrows indicate the autophagosomes. Values are expressed as the mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, LC3B light chain 3 beta, ACTB β-actin, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Journal: Military Medical Research

    Article Title: Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo

    doi: 10.1186/s40779-022-00369-0

    Figure Lengend Snippet: UTMD-induced autophagosome accumulation in IR-exposed glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s. Then, the cells were exposed to IR (2 Gy), and 24 h later, the level of LC3B2 was detected by Western blotting analysis and the indicated protein was quantified. c GL261 cells were transfected with a plasmid expressing GFP-LC3B. After 24 h, the cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Following fixation, the cells were immediately visualized by confocal microscopy, and the number of GFP-LC3B dots in each cell was counted. d GL261 cells were pretreated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s). Then, the cells were exposed to IR (2 Gy) and incubated for another 24 h. Autophagosomes were detected by transmission electron microscopy. Arrows indicate the autophagosomes. Values are expressed as the mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, LC3B light chain 3 beta, ACTB β-actin, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Article Snippet: The protein bands were visualized using an enhanced chemiluminescence system, and densitometric analysis was performed using Scion Image-Release Beta 4.02 software ( http://scion-corporation.software.informer.com ).

    Techniques: Western Blot, Transfection, Plasmid Preparation, Expressing, Incubation, Confocal Microscopy, Transmission Assay, Electron Microscopy, Standard Deviation

    UTMD inhibited autophagic flux in IR-treated glioblastoma cells. a , b Representative immunoblot and quantification analysis of p62 after GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s followed by IR (2 Gy) exposure. ACTB was used as an internal standard for protein loading. c , d GL261 and U251 cells were pretreated with RAPA (20 nmol/L) or BafA1 (10 nmol/L) for 1 h and then cells were treated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. Total cell lysates were immunoblotted with anti-p62, anti-LC3B, and anti-ACTB antibodies and the bar graphs show the quantification of LC3B2 and p62. e–h GL261 and U251 cells were transfected with lentiviral vectors encoding ATG5 or ATG5 siRNA . Then, the cells were treated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. The expression of LC3B2, p62 and ATG5 was detected by Western blotting. The bar graphs show the quantification of LC3B2, p62 and ATG5. i , j GL261 and U251 cells were pretreated with 3-MA (5 mmol/L) for 1 h and then exposed to UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. Total cell lysates were immunoblotted with anti-p62, anti-LC3B, and anti-ACTB antibodies. The bar graphs show the quantification of LC3B2 and p62. Values are expressed as the mean ± SD ( n = 3). * P < 0.05, ** P < 0.01 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group; & P < 0.05, && P < 0.05 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, ACTB β-actin, LC3B light chain 3 beta, p62 sequestosome 1, RAPA rapamycin, BafA1 bafilomycin A1, 3-MA 3-methyladenine, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Journal: Military Medical Research

    Article Title: Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo

    doi: 10.1186/s40779-022-00369-0

    Figure Lengend Snippet: UTMD inhibited autophagic flux in IR-treated glioblastoma cells. a , b Representative immunoblot and quantification analysis of p62 after GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs) at a duty cycle of 10% for 60 s followed by IR (2 Gy) exposure. ACTB was used as an internal standard for protein loading. c , d GL261 and U251 cells were pretreated with RAPA (20 nmol/L) or BafA1 (10 nmol/L) for 1 h and then cells were treated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. Total cell lysates were immunoblotted with anti-p62, anti-LC3B, and anti-ACTB antibodies and the bar graphs show the quantification of LC3B2 and p62. e–h GL261 and U251 cells were transfected with lentiviral vectors encoding ATG5 or ATG5 siRNA . Then, the cells were treated with UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. The expression of LC3B2, p62 and ATG5 was detected by Western blotting. The bar graphs show the quantification of LC3B2, p62 and ATG5. i , j GL261 and U251 cells were pretreated with 3-MA (5 mmol/L) for 1 h and then exposed to UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. Total cell lysates were immunoblotted with anti-p62, anti-LC3B, and anti-ACTB antibodies. The bar graphs show the quantification of LC3B2 and p62. Values are expressed as the mean ± SD ( n = 3). * P < 0.05, ** P < 0.01 vs. the vehicle-treated control group; # P < 0.05, ## P < 0.01 vs. IR group; & P < 0.05, && P < 0.05 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, ACTB β-actin, LC3B light chain 3 beta, p62 sequestosome 1, RAPA rapamycin, BafA1 bafilomycin A1, 3-MA 3-methyladenine, GFP green fluorescent protein, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Article Snippet: The protein bands were visualized using an enhanced chemiluminescence system, and densitometric analysis was performed using Scion Image-Release Beta 4.02 software ( http://scion-corporation.software.informer.com ).

    Techniques: Western Blot, Transfection, Expressing, Standard Deviation

    UTMD inhibited autophagosome fusion with lysosomes in IR-treated glioblastoma cells. GL261 cells were transfected with RFP-GFP-LC3B for 24 h and then exposed to UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. a Representative images of fluorescent LC3 puncta are shown. b Mean numbers of GFP and RFP dots/cell (top). Mean number of autophagosomes (yellow dots in merged images) and autolysosomes (red dots in merged images)/cell (bottom). Values are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group. GFP green fluorescent protein, RFP red fluorescent protein, LC3B light chain 3 beta, IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, MBs microbubbles, SD standard deviation

    Journal: Military Medical Research

    Article Title: Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo

    doi: 10.1186/s40779-022-00369-0

    Figure Lengend Snippet: UTMD inhibited autophagosome fusion with lysosomes in IR-treated glioblastoma cells. GL261 cells were transfected with RFP-GFP-LC3B for 24 h and then exposed to UTMD (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs at a duty cycle of 10% for 60 s) followed by IR (2 Gy) exposure. a Representative images of fluorescent LC3 puncta are shown. b Mean numbers of GFP and RFP dots/cell (top). Mean number of autophagosomes (yellow dots in merged images) and autolysosomes (red dots in merged images)/cell (bottom). Values are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group. GFP green fluorescent protein, RFP red fluorescent protein, LC3B light chain 3 beta, IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, MBs microbubbles, SD standard deviation

    Article Snippet: The protein bands were visualized using an enhanced chemiluminescence system, and densitometric analysis was performed using Scion Image-Release Beta 4.02 software ( http://scion-corporation.software.informer.com ).

    Techniques: Transfection, Standard Deviation

    UTMD inhibited PGRMC1 expression and binding with LC3B in IR-treated glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs), and then the cells were exposed to IR (2 Gy). PGRMC1 expression was measured by Western blotting. c GL261 and U251 cells were pretreated with UTMD. Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Immunofluorescence staining analysis of PGRMC1 (green) and LC3B (red) expression, the nuclei were stained with DAPI (blue). Values are expressed as mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, ACTB β-actin, LC3B light chain 3 beta, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Journal: Military Medical Research

    Article Title: Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo

    doi: 10.1186/s40779-022-00369-0

    Figure Lengend Snippet: UTMD inhibited PGRMC1 expression and binding with LC3B in IR-treated glioblastoma cells. a , b GL261 and U251 cells were treated with UTMD-L (ultrasonic intensity of 1.2 W/cm 2 combined with 100 μl/ml MBs) or UTMD-H (ultrasonic intensity of 1.2 W/cm 2 combined with 200 μl/ml MBs), and then the cells were exposed to IR (2 Gy). PGRMC1 expression was measured by Western blotting. c GL261 and U251 cells were pretreated with UTMD. Then, the cells were exposed to IR (2 Gy) and incubated for an additional 24 h. Immunofluorescence staining analysis of PGRMC1 (green) and LC3B (red) expression, the nuclei were stained with DAPI (blue). Values are expressed as mean ± SD ( n = 3). * P < 0.05 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, ACTB β-actin, LC3B light chain 3 beta, MBs microbubbles, SD standard deviation, a.u. arbitrary units

    Article Snippet: The protein bands were visualized using an enhanced chemiluminescence system, and densitometric analysis was performed using Scion Image-Release Beta 4.02 software ( http://scion-corporation.software.informer.com ).

    Techniques: Expressing, Binding Assay, Western Blot, Incubation, Immunofluorescence, Staining, Standard Deviation

    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

    Journal: Military Medical Research

    Article Title: Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo

    doi: 10.1186/s40779-022-00369-0

    Figure Lengend Snippet: 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

    Article Snippet: The protein bands were visualized using an enhanced chemiluminescence system, and densitometric analysis was performed using Scion Image-Release Beta 4.02 software ( http://scion-corporation.software.informer.com ).

    Techniques: Western Blot, Transfection, Expressing, Standard Deviation

    UTMD enhanced the radiosensitivity of glioblastoma via inhibiting PGRMC1-mediated autophagy in mice. Six-week-old female C57BL/6J mice were inoculated in the right caudate putamen with GL261 cells (1 × 10 5 cells per mouse) with or without shPGRMC1-expressing vector to establish the orthotopic glioblastoma mouse model. Seven days after transplantation, the tumor size was evaluated by in vivo bioluminescent imaging. Then, the animals were randomly allocated to treatment groups to receive control treatment or IR (every day, 2 Gy/fraction, 5 fractions) combined with or without UTMD (every other day) treatment over a period of 5 d. On day 20 after tumor transplantation, US and bioluminescent imaging were used to determine the tumor size. Meanwhile, mice were euthanized, and brain tumors were collected. In vivo bioluminescent images (a) and quantification of orthotopic glioblastoma tumors (b) in the brains of mice. c Kaplan–Meier survival analysis of orthotopic glioblastoma-bearing mice. d Orthotopic glioblastoma tumor size was determined by US. White circles indicate tumors. e Immunofluorescent staining and the quantification of Ki67 (green) in orthotopic glioblastoma tumors in the brains of mice. f Tumor tissues were harvested on day 20 after tumor implantation and lysed, and Western blotting analysis was performed. The expression of LC3B2, p62, and PGRMC1 were measured. g The bar graphs showed the quantification of LC3B2, p62, and PGRMC1. Values are expressed as mean ± SD ( n = 6). * P < 0.05 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group; & P < 0.05 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, LC3B light chain 3 beta, p62 sequestosome 1, ACTB β-actin, SD standard deviation, p/s/cm 2 /sr photon per second per square centimetre per steradian, a.u. arbitrary units

    Journal: Military Medical Research

    Article Title: Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo

    doi: 10.1186/s40779-022-00369-0

    Figure Lengend Snippet: UTMD enhanced the radiosensitivity of glioblastoma via inhibiting PGRMC1-mediated autophagy in mice. Six-week-old female C57BL/6J mice were inoculated in the right caudate putamen with GL261 cells (1 × 10 5 cells per mouse) with or without shPGRMC1-expressing vector to establish the orthotopic glioblastoma mouse model. Seven days after transplantation, the tumor size was evaluated by in vivo bioluminescent imaging. Then, the animals were randomly allocated to treatment groups to receive control treatment or IR (every day, 2 Gy/fraction, 5 fractions) combined with or without UTMD (every other day) treatment over a period of 5 d. On day 20 after tumor transplantation, US and bioluminescent imaging were used to determine the tumor size. Meanwhile, mice were euthanized, and brain tumors were collected. In vivo bioluminescent images (a) and quantification of orthotopic glioblastoma tumors (b) in the brains of mice. c Kaplan–Meier survival analysis of orthotopic glioblastoma-bearing mice. d Orthotopic glioblastoma tumor size was determined by US. White circles indicate tumors. e Immunofluorescent staining and the quantification of Ki67 (green) in orthotopic glioblastoma tumors in the brains of mice. f Tumor tissues were harvested on day 20 after tumor implantation and lysed, and Western blotting analysis was performed. The expression of LC3B2, p62, and PGRMC1 were measured. g The bar graphs showed the quantification of LC3B2, p62, and PGRMC1. Values are expressed as mean ± SD ( n = 6). * P < 0.05 vs. the vehicle-treated control group; ## P < 0.01 vs. IR group; & P < 0.05 vs. IR plus UTMD group. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, LC3B light chain 3 beta, p62 sequestosome 1, ACTB β-actin, SD standard deviation, p/s/cm 2 /sr photon per second per square centimetre per steradian, a.u. arbitrary units

    Article Snippet: The protein bands were visualized using an enhanced chemiluminescence system, and densitometric analysis was performed using Scion Image-Release Beta 4.02 software ( http://scion-corporation.software.informer.com ).

    Techniques: Expressing, Plasmid Preparation, Transplantation Assay, In Vivo, Imaging, Staining, Tumor Implantation, Western Blot, Standard Deviation

    UTMD enhanced the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy. UTMD improved the response of glioblastoma cells to IR via the proposed signaling pathways: UTMD downregulates PGRMC1 expression, thereby inhibiting the combination of PGRMC1 with LC3B2, which is followed by a decrease of autophagosome-lysosome fusion, subsequently disrupting autophagic degradation and ultimately enhancing the radiosensitivity of glioblastoma. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, LC3B light chain 3 beta

    Journal: Military Medical Research

    Article Title: Ultrasound-triggered microbubble destruction enhances the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy in vitro and in vivo

    doi: 10.1186/s40779-022-00369-0

    Figure Lengend Snippet: UTMD enhanced the radiosensitivity of glioblastoma by inhibiting PGRMC1-mediated autophagy. UTMD improved the response of glioblastoma cells to IR via the proposed signaling pathways: UTMD downregulates PGRMC1 expression, thereby inhibiting the combination of PGRMC1 with LC3B2, which is followed by a decrease of autophagosome-lysosome fusion, subsequently disrupting autophagic degradation and ultimately enhancing the radiosensitivity of glioblastoma. IR ionizing radiation, UTMD ultrasound-triggered microbubble destruction, PGRMC1 progesterone receptor membrane component 1, LC3B light chain 3 beta

    Article Snippet: The protein bands were visualized using an enhanced chemiluminescence system, and densitometric analysis was performed using Scion Image-Release Beta 4.02 software ( http://scion-corporation.software.informer.com ).

    Techniques: Expressing