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inhibitor negative control inhibitor nc  (MedChemExpress)
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Inhibitor Negative Control Inhibitor Nc, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mir 1231 inhibitor nc  (General Biosystems Inc)
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CircRAD18 acts as a sponge <t>for</t> <t>miR-1231</t> in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.
Mir 1231 Inhibitor Nc, supplied by General Biosystems Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/nc+inhibitor/1231+inhibitor+mir+nc/pmc13178732-111-24-32
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inhibitor nc  (Sangon Biotech)
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CircRAD18 acts as a sponge <t>for</t> <t>miR-1231</t> in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.
Inhibitor Nc, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/nc+inhibitor/control+negative+sirna/pm42275918-73-16-25
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control nc inhibitor  (General Biosystems Inc)
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CircRAD18 acts as a sponge <t>for</t> <t>miR-1231</t> in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.
Control Nc Inhibitor, supplied by General Biosystems Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nc mimics r04602  (MedChemExpress)
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CircRAD18 acts as a sponge <t>for</t> <t>miR-1231</t> in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.
Nc Mimics R04602, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mimics inhibitor nc  (Genechem)
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Genechem mimics inhibitor nc
CircRAD18 acts as a sponge <t>for</t> <t>miR-1231</t> in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.
Mimics Inhibitor Nc, supplied by Genechem, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/nc+inhibitor/inhibitor+mimics+nc+relative/pm41931957-63-17-29
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inhibitor nc mir inhibitor pcdna3 1 nc pcdna3 1 igf1r  (MedChemExpress)
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MedChemExpress inhibitor nc mir inhibitor pcdna3 1 nc pcdna3 1 igf1r
CircRAD18 acts as a sponge <t>for</t> <t>miR-1231</t> in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.
Inhibitor Nc Mir Inhibitor Pcdna3 1 Nc Pcdna3 1 Igf1r, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mirna 1290 inhibitor nc  (Sangon Biotech)
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Sangon Biotech mirna 1290 inhibitor nc
CircRAD18 acts as a sponge <t>for</t> <t>miR-1231</t> in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.
Mirna 1290 Inhibitor Nc, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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CircRAD18 acts as a sponge for miR-1231 in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.

Journal: International Journal of Molecular Medicine

Article Title: CircRAD18 promotes glioblastoma proliferation, migration and invasion via the miR-1231/LUC7L2 axis

doi: 10.3892/ijmm.2026.5851

Figure Lengend Snippet: CircRAD18 acts as a sponge for miR-1231 in GBM cells. (A) Venn diagram showing miRNA targets of circRAD18 predicted using the CircBank and CircInteractome databases. (B) Volcano plot showing differentially expressed miRNAs in GBM cells, including 373 upregulated and 807 downregulated. (C) Venn diagram illustrating the overlap between predicted miRNAs and downregulated miRNAs from the GSE90603 dataset. (D) Data from the CGGA database showing that miR-1231 expression decreased as glioma grade increased. (E) Using data from the CGGA database, patients were categorized by miR-1231 levels and generated Kaplan-Meier survival curves to compare survival rates between the two groups. (F) FISH was used to detect the co-localization of circRAD18 and miR-1231 in the cytoplasm of GBM cells. circRAD18 is shown in red, miR-1231 in green, and nuclei are stained blue with DAPI. Scale bar, 20 μ m. Nucleocytoplasmic fractionation analysis followed by RT-qPCR demonstrated that miR-1231 was predominantly localized in the cytoplasm of (G) U87 and (H) U251 cells. β-actin and U6 were used as cytoplasmic and nuclear markers, respectively, to validate the fractionation efficiency. (I) Predicted binding sites of miR-1231 in circRAD18, with the Mut version of circRAD18 presented. (J) The dual-luciferase reporter assay determining the binding between circRAD18 and miR-1231. (K) RNA pull-down assay performed to verify the direct binding between circRAD18 and miR-1231. (L) RT-qPCR showed that circRAD18 knockdown markedly increased miR-1231 expression in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; CGGA, Chinese Glioma Genome Atlas; FISH, fluorescence in situ hybridization; RT-qPCR, reverse transcription-quantitative PCR; MUT, mutant; WT, wild type.

Article Snippet: The small interfering RNAs (siRNAs) investigated in the present study included si1-circRAD18, si2-circRAD18, circRAD18-negative control (NC), miR-1231 mimic, miR-1231 mimic NC, miR-1231 inhibitor and miR-1231 inhibitor NC, all designed and synthesized by General Biosystems (Anhui) Co., Ltd.

Techniques: Expressing, Generated, Staining, Fractionation, Quantitative RT-PCR, Binding Assay, Luciferase, Reporter Assay, Pull Down Assay, Knockdown, Fluorescence, In Situ Hybridization, Reverse Transcription, Real-time Polymerase Chain Reaction, Mutagenesis

miR-1231 directly targets LUC7L2. (A) Venn diagram showing predicted miR-1231 target mRNAs using TargetScan, miRWalk and mirDIP databases. (B) Volcano plot showing differentially expressed mRNAs in GBM cells, with 2,499 upregulated and 3,324 downregulated. (C) Venn diagram illustrating the overlap between predicted mRNAs and upregulated mRNAs from the GSE4290 dataset. (D) Data from the CGGA database indicating that LUC7L2 expression increased with glioma grade. (E) Using data from the CGGA database, patients were categorized by LUC7L2 levels and generated Kaplan-Meier survival curves to compare the survival rates between the two groups. (F) Predicted binding sites of miR-1231 in LUC7L2 3'-UTR, with the Mut version of LUC7L2 3'-UTR presented. (G) The dual-luciferase reporter assay confirming the binding between miR-1231 and LUC7L2. (H) Western blot analysis showing that miR-1231 mimic treatment reduced LUC7L2 protein levels in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001. miRNA, microRNA; GBM, glioblastoma; CGGA, Chinese Glioma Genome Atlas; NC, negative control; MUT, mutant; WT, wild type.

Journal: International Journal of Molecular Medicine

Article Title: CircRAD18 promotes glioblastoma proliferation, migration and invasion via the miR-1231/LUC7L2 axis

doi: 10.3892/ijmm.2026.5851

Figure Lengend Snippet: miR-1231 directly targets LUC7L2. (A) Venn diagram showing predicted miR-1231 target mRNAs using TargetScan, miRWalk and mirDIP databases. (B) Volcano plot showing differentially expressed mRNAs in GBM cells, with 2,499 upregulated and 3,324 downregulated. (C) Venn diagram illustrating the overlap between predicted mRNAs and upregulated mRNAs from the GSE4290 dataset. (D) Data from the CGGA database indicating that LUC7L2 expression increased with glioma grade. (E) Using data from the CGGA database, patients were categorized by LUC7L2 levels and generated Kaplan-Meier survival curves to compare the survival rates between the two groups. (F) Predicted binding sites of miR-1231 in LUC7L2 3'-UTR, with the Mut version of LUC7L2 3'-UTR presented. (G) The dual-luciferase reporter assay confirming the binding between miR-1231 and LUC7L2. (H) Western blot analysis showing that miR-1231 mimic treatment reduced LUC7L2 protein levels in U87 and U251 cells. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001. miRNA, microRNA; GBM, glioblastoma; CGGA, Chinese Glioma Genome Atlas; NC, negative control; MUT, mutant; WT, wild type.

Article Snippet: The small interfering RNAs (siRNAs) investigated in the present study included si1-circRAD18, si2-circRAD18, circRAD18-negative control (NC), miR-1231 mimic, miR-1231 mimic NC, miR-1231 inhibitor and miR-1231 inhibitor NC, all designed and synthesized by General Biosystems (Anhui) Co., Ltd.

Techniques: Expressing, Generated, Binding Assay, Luciferase, Reporter Assay, Western Blot, Negative Control, Mutagenesis

circRAD18 promotes the proliferation, migration and invasion of GBM cells by sponging miR-1231. CCK-8 assays showing that miR-1231 inhibitor transfection promoted the proliferation of (A) U87 and (B) U251 cells. Wound healing assays showing that miR-1231 inhibitor transfection enhanced the migration of (C) U87 and (D) U251 cells. Scale bar, 100 μ m. (E) Transwell assays showed that miR-1231 inhibitor transfection promoted the invasion of U87 and U251 cells. Scale bar, 100 μ m. CCK-8 assays showing that si-circRAD18 co-transfection attenuated the proliferation-promoting effect of miR-1231 inhibitor in (F) U87 and (G) U251 cells. Wound healing assays showing that si-circRAD18 co-transfection attenuated the migration-promoting effect of miR-1231 inhibitor in (H) U87 and (I) U251 cells. Scale bar, 100 μ m. (J) Transwell assays showing that si-circRAD18 co-transfection attenuated the invasion-promoting effect of miR-1231 inhibitor in U87 and U251 cells. Scale bar, 100 μ m. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; si, small interfering.

Journal: International Journal of Molecular Medicine

Article Title: CircRAD18 promotes glioblastoma proliferation, migration and invasion via the miR-1231/LUC7L2 axis

doi: 10.3892/ijmm.2026.5851

Figure Lengend Snippet: circRAD18 promotes the proliferation, migration and invasion of GBM cells by sponging miR-1231. CCK-8 assays showing that miR-1231 inhibitor transfection promoted the proliferation of (A) U87 and (B) U251 cells. Wound healing assays showing that miR-1231 inhibitor transfection enhanced the migration of (C) U87 and (D) U251 cells. Scale bar, 100 μ m. (E) Transwell assays showed that miR-1231 inhibitor transfection promoted the invasion of U87 and U251 cells. Scale bar, 100 μ m. CCK-8 assays showing that si-circRAD18 co-transfection attenuated the proliferation-promoting effect of miR-1231 inhibitor in (F) U87 and (G) U251 cells. Wound healing assays showing that si-circRAD18 co-transfection attenuated the migration-promoting effect of miR-1231 inhibitor in (H) U87 and (I) U251 cells. Scale bar, 100 μ m. (J) Transwell assays showing that si-circRAD18 co-transfection attenuated the invasion-promoting effect of miR-1231 inhibitor in U87 and U251 cells. Scale bar, 100 μ m. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; si, small interfering.

Article Snippet: The small interfering RNAs (siRNAs) investigated in the present study included si1-circRAD18, si2-circRAD18, circRAD18-negative control (NC), miR-1231 mimic, miR-1231 mimic NC, miR-1231 inhibitor and miR-1231 inhibitor NC, all designed and synthesized by General Biosystems (Anhui) Co., Ltd.

Techniques: Migration, CCK-8 Assay, Transfection, Cotransfection

circRAD18 promotes the proliferation, migration and invasion of GBM cells through the miR-1231/LUC7L2 axis. (A) Western blot analysis showing that circRAD18 knockdown reduced LUC7L2 protein levels in U87 and U251 cells. (B) Western blot analysis showing that miR-1231 inhibitor increased LUC7L2 protein levels in U87 and U251 cells. (C) Western blot analysis showing that si-circRAD18 co-transfection attenuated the increase in LUC7L2 protein levels induced by miR-1231 inhibitor in U87 and U251 cells. (D) Western blot analysis showing that LUC7L2 overexpression increased LUC7L2 protein levels in U87 and U251 cells. (E) RT-qPCR analysis showing that LUC7L2 overexpression increased LUC7L2 expression in U87 and U251 cells. CCK-8 assays showing that LUC7L2 overexpression promoted the proliferation of (F) U87 and (G) U251 cells. Wound healing assays showing that LUC7L2 overexpression enhanced the migration of (H) U87 and (I) U251 cells. Scale bar, 100 μ m. (J) Transwell assays showing that LUC7L2 overexpression promoted the invasion of U87 and U251 cells. Scale bar, 100 μ m. CCK-8 assays showing that circRAD18 knockdown attenuated the proliferation-promoting effect of LUC7L2 overexpression in (K) U87 and (L) U251 cells. Wound healing assays showing that circRAD18 knockdown attenuated the migration-promoting effect of LUC7L2 overexpression in (M) U87 and (N) U251 cells. Scale bar, 100 μ m. (O) Transwell assays showed that circRAD18 knockdown attenuated the invasion-promoting effect of LUC7L2 overexpression in U87 and U251 cells. Scale bar, 100 μ m. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; si, small interfering; RT-qPCR, reverse transcription-quantitative PCR; OE, overexpressed; NC, negative control.

Journal: International Journal of Molecular Medicine

Article Title: CircRAD18 promotes glioblastoma proliferation, migration and invasion via the miR-1231/LUC7L2 axis

doi: 10.3892/ijmm.2026.5851

Figure Lengend Snippet: circRAD18 promotes the proliferation, migration and invasion of GBM cells through the miR-1231/LUC7L2 axis. (A) Western blot analysis showing that circRAD18 knockdown reduced LUC7L2 protein levels in U87 and U251 cells. (B) Western blot analysis showing that miR-1231 inhibitor increased LUC7L2 protein levels in U87 and U251 cells. (C) Western blot analysis showing that si-circRAD18 co-transfection attenuated the increase in LUC7L2 protein levels induced by miR-1231 inhibitor in U87 and U251 cells. (D) Western blot analysis showing that LUC7L2 overexpression increased LUC7L2 protein levels in U87 and U251 cells. (E) RT-qPCR analysis showing that LUC7L2 overexpression increased LUC7L2 expression in U87 and U251 cells. CCK-8 assays showing that LUC7L2 overexpression promoted the proliferation of (F) U87 and (G) U251 cells. Wound healing assays showing that LUC7L2 overexpression enhanced the migration of (H) U87 and (I) U251 cells. Scale bar, 100 μ m. (J) Transwell assays showing that LUC7L2 overexpression promoted the invasion of U87 and U251 cells. Scale bar, 100 μ m. CCK-8 assays showing that circRAD18 knockdown attenuated the proliferation-promoting effect of LUC7L2 overexpression in (K) U87 and (L) U251 cells. Wound healing assays showing that circRAD18 knockdown attenuated the migration-promoting effect of LUC7L2 overexpression in (M) U87 and (N) U251 cells. Scale bar, 100 μ m. (O) Transwell assays showed that circRAD18 knockdown attenuated the invasion-promoting effect of LUC7L2 overexpression in U87 and U251 cells. Scale bar, 100 μ m. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; miRNA, microRNA; si, small interfering; RT-qPCR, reverse transcription-quantitative PCR; OE, overexpressed; NC, negative control.

Article Snippet: The small interfering RNAs (siRNAs) investigated in the present study included si1-circRAD18, si2-circRAD18, circRAD18-negative control (NC), miR-1231 mimic, miR-1231 mimic NC, miR-1231 inhibitor and miR-1231 inhibitor NC, all designed and synthesized by General Biosystems (Anhui) Co., Ltd.

Techniques: Migration, Western Blot, Knockdown, Cotransfection, Over Expression, Quantitative RT-PCR, Expressing, CCK-8 Assay, Reverse Transcription, Real-time Polymerase Chain Reaction, Negative Control

circRAD18 knockdown inhibits GBM progression in vivo . (A and B) Representative images of xenograft tumors in nude mice showing that circRAD18 knockdown reduced tumor growth. (C) Tumor growth curves showing that circRAD18 knockdown slowed the growth of subcutaneous xenograft tumors. (D) Tumor volume measurements at day 28 showing that circRAD18 knockdown reduced tumor size compared with the control group. (E) Tumor weights measured on day 28 showing that circRAD18 knockdown decreased tumor mass compared with the control group. (F) RT-qPCR analysis showing that circRAD18 knockdown decreased circRAD18 expression in xenograft tumors. (G) RT-qPCR analysis showing that circRAD18 knockdown increased miR-1231 expression in xenograft tumors. (H) RT-qPCR analysis showing that circRAD18 knockdown decreased LUC7L2 expression in xenograft tumors. (I) IHC staining of xenograft tumors showing that circRAD18 knockdown decreased LUC7L2 protein levels. Scale bar, 100 μ m. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; IHC, immunohistochemistry; RT-qPCR, reverse transcription-quantitative PCR; sh, short hairpin.

Journal: International Journal of Molecular Medicine

Article Title: CircRAD18 promotes glioblastoma proliferation, migration and invasion via the miR-1231/LUC7L2 axis

doi: 10.3892/ijmm.2026.5851

Figure Lengend Snippet: circRAD18 knockdown inhibits GBM progression in vivo . (A and B) Representative images of xenograft tumors in nude mice showing that circRAD18 knockdown reduced tumor growth. (C) Tumor growth curves showing that circRAD18 knockdown slowed the growth of subcutaneous xenograft tumors. (D) Tumor volume measurements at day 28 showing that circRAD18 knockdown reduced tumor size compared with the control group. (E) Tumor weights measured on day 28 showing that circRAD18 knockdown decreased tumor mass compared with the control group. (F) RT-qPCR analysis showing that circRAD18 knockdown decreased circRAD18 expression in xenograft tumors. (G) RT-qPCR analysis showing that circRAD18 knockdown increased miR-1231 expression in xenograft tumors. (H) RT-qPCR analysis showing that circRAD18 knockdown decreased LUC7L2 expression in xenograft tumors. (I) IHC staining of xenograft tumors showing that circRAD18 knockdown decreased LUC7L2 protein levels. Scale bar, 100 μ m. All data are presented as mean ± SEM and each experiment was performed in triplicate. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. circ, circular RNA; GBM, glioblastoma; IHC, immunohistochemistry; RT-qPCR, reverse transcription-quantitative PCR; sh, short hairpin.

Article Snippet: The small interfering RNAs (siRNAs) investigated in the present study included si1-circRAD18, si2-circRAD18, circRAD18-negative control (NC), miR-1231 mimic, miR-1231 mimic NC, miR-1231 inhibitor and miR-1231 inhibitor NC, all designed and synthesized by General Biosystems (Anhui) Co., Ltd.

Techniques: Knockdown, In Vivo, Control, Quantitative RT-PCR, Expressing, Immunohistochemistry, Reverse Transcription, Real-time Polymerase Chain Reaction