u87 (ATCC)

ATCC u87

RFC2 expression is upregulated in GBM tissues and cells. (A) RT-qPCR analysis of gene expression of RFC2 in GBM tumor tissues (n=39) and adjacent controls (n=39) from patients with GBM. **P<0.001, compared with Normal group using paired Student's t-test. (B) RT-qPCR analysis of the RFC2 expression in GBM cell lines (U251, <t>U87,</t> SHG44 and A172) and the normal astrocyte NHA cell line. **P<0.001, compared with NHA using one-way ANOVA with Dunnett's test. (C) RT-qPCR analysis of gene expression of RFC2 in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2. (D) Western blot analysis of RFC2 protein expression in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2. (C and D) **P<0.001, compared with CON using one-way ANOVA with Dunnett's test. CON, blank control; si-NC, si-RFC2 negative control; OE-NC, pcDNA 3.1 empty vector; Co-NC, si-NC+OE-NC; si-RFC2, siRNA-RFC2; RFC2-OE, RFC2-overexpression; RFC2, replication factor C subunit 2; GBM, glioblastoma; RT-q, reverse transcription-quantitative; si(RNA), small interfering; OE, overexpression; NC, negative control.

U87, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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u 87 mg atcc htb 14 glio blastoma (ATCC)

ATCC u 87 mg atcc htb 14 glio blastoma

U 87 Mg Atcc Htb 14 Glio Blastoma, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human glioma cell lines u87 mg (Ubigene Biosciences Co Ltd)

Ubigene Biosciences Co Ltd human glioma cell lines u87 mg
$lncRNA DDX11-AS1 expression is upregulated in human glioma specimens. ( A ) Expression of lncRNA DDX11-AS1 was evaluated in 32 glioma tissues and 12 normal brain tissues by RT-qPCR. ( B ) Expression of lncRNA DDX11-AS1 was identified in 9 low-grade glioma (LGG) tissues and 23 glioblastoma (GBM) tissues by RT-qPCR. ( C ) lncRNA DDX11-AS1 expression level in open-access datasets of TCGA and GTEx ( n = 1152 for normal brain tissues and n = 689 for glioblastoma). ( D ) Kaplan-Meier plots of overall survival in glioma patients with high ( n = 337) and low ( n = 336) levels of DDX11-AS1 in the TCGA database. ( E ) Kaplan-Meier plots of overall survival in glioma patients with high ( n = 113) and low ( n = 109) levels of DDX11-AS1 in the CGGA database. ( F ) Expression of lncRNA DDX11-AS1 in HEB cells and four glioma cell lines ( n = 6). ( G , H ) Levels of DDX11-AS1 in the nuclear and cytoplasmic fractions of <t>U87</t> and U251 cells ( n = 6). Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test$
Human Glioma Cell Lines U87 Mg, supplied by Ubigene Biosciences Co Ltd, 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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human glioma cell lines u87 mg - by Bioz Stars, 2026-10

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human glioma cell lines (ATCC)

ATCC human glioma cell lines
$lncRNA DDX11-AS1 expression is upregulated in human glioma specimens. ( A ) Expression of lncRNA DDX11-AS1 was evaluated in 32 glioma tissues and 12 normal brain tissues by RT-qPCR. ( B ) Expression of lncRNA DDX11-AS1 was identified in 9 low-grade glioma (LGG) tissues and 23 glioblastoma (GBM) tissues by RT-qPCR. ( C ) lncRNA DDX11-AS1 expression level in open-access datasets of TCGA and GTEx ( n = 1152 for normal brain tissues and n = 689 for glioblastoma). ( D ) Kaplan-Meier plots of overall survival in glioma patients with high ( n = 337) and low ( n = 336) levels of DDX11-AS1 in the TCGA database. ( E ) Kaplan-Meier plots of overall survival in glioma patients with high ( n = 113) and low ( n = 109) levels of DDX11-AS1 in the CGGA database. ( F ) Expression of lncRNA DDX11-AS1 in HEB cells and four glioma cell lines ( n = 6). ( G , H ) Levels of DDX11-AS1 in the nuclear and cytoplasmic fractions of <t>U87</t> and U251 cells ( n = 6). Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test$
Human Glioma Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/unknown+origin+u87/A-172/pmc11015917-97-0-9
Average 97 stars, based on 1 article reviews

human glioma cell lines - by Bioz Stars, 2026-10

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Image Search Results

Journal: Oncology Letters

Article Title: MicroRNA-744-5p inhibits glioblastoma malignancy by suppressing replication factor C subunit 2

doi: 10.3892/ol.2021.12869

Figure Lengend Snippet: RFC2 expression is upregulated in GBM tissues and cells. (A) RT-qPCR analysis of gene expression of RFC2 in GBM tumor tissues (n=39) and adjacent controls (n=39) from patients with GBM. **P<0.001, compared with Normal group using paired Student's t-test. (B) RT-qPCR analysis of the RFC2 expression in GBM cell lines (U251, U87, SHG44 and A172) and the normal astrocyte NHA cell line. **P<0.001, compared with NHA using one-way ANOVA with Dunnett's test. (C) RT-qPCR analysis of gene expression of RFC2 in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2. (D) Western blot analysis of RFC2 protein expression in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2. (C and D) **P<0.001, compared with CON using one-way ANOVA with Dunnett's test. CON, blank control; si-NC, si-RFC2 negative control; OE-NC, pcDNA 3.1 empty vector; Co-NC, si-NC+OE-NC; si-RFC2, siRNA-RFC2; RFC2-OE, RFC2-overexpression; RFC2, replication factor C subunit 2; GBM, glioblastoma; RT-q, reverse transcription-quantitative; si(RNA), small interfering; OE, overexpression; NC, negative control.

Article Snippet: The human GBM cell lines, U87 (cat. no. HTB-14; GBM of unknown origin) and A172 (cat. no. CRL-1620) were purchased from the American Type Culture Collection.

Techniques: Expressing, Quantitative RT-PCR, Gene Expression, Transfection, Western Blot, Control, Negative Control, Plasmid Preparation, Over Expression, Reverse Transcription

RFC2 promotes cellular proliferation, migration and adhesion, and suppresses cell apoptosis in glioblastoma. (A) Viability of U251 and U87 cells transfected with NC, RFC2-OE and Si-RFC2 was determined by Cell Counting Kit 8 assay. (B) Cellular proliferation was detected in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2 by BrdU assay. (C) Wound-healing assay was performed in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2. (D) Adhesion ability was detected in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2. (E) Caspase3 activity was determined in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2 by caspase3 activity assay kit. (F) Protein expression levels of Bax and Bcl-2 were determined in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2 by western blotting. *P<0.05 and **P<0.001, compared with CON using one-way ANOVA with Dunnett's test. CON, blank control; NC, negative control; si-RFC2, siRNA-RFC2; RFC2-OE, RFC2-overexpression; RFC2, replication factor C subunit 2.

Journal: Oncology Letters

Article Title: MicroRNA-744-5p inhibits glioblastoma malignancy by suppressing replication factor C subunit 2

doi: 10.3892/ol.2021.12869

Figure Lengend Snippet: RFC2 promotes cellular proliferation, migration and adhesion, and suppresses cell apoptosis in glioblastoma. (A) Viability of U251 and U87 cells transfected with NC, RFC2-OE and Si-RFC2 was determined by Cell Counting Kit 8 assay. (B) Cellular proliferation was detected in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2 by BrdU assay. (C) Wound-healing assay was performed in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2. (D) Adhesion ability was detected in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2. (E) Caspase3 activity was determined in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2 by caspase3 activity assay kit. (F) Protein expression levels of Bax and Bcl-2 were determined in U251 and U87 cells transfected with NC, RFC2-OE and si-RFC2 by western blotting. *P<0.05 and **P<0.001, compared with CON using one-way ANOVA with Dunnett's test. CON, blank control; NC, negative control; si-RFC2, siRNA-RFC2; RFC2-OE, RFC2-overexpression; RFC2, replication factor C subunit 2.

Article Snippet: The human GBM cell lines, U87 (cat. no. HTB-14; GBM of unknown origin) and A172 (cat. no. CRL-1620) were purchased from the American Type Culture Collection.

Techniques: Migration, Transfection, Cell Counting, BrdU Staining, Wound Healing Assay, Activity Assay, Caspase-3 Activity Assay, Expressing, Western Blot, Control, Negative Control, Over Expression

RFC2 is a direct target of miR-744-5p in GBM. (A) Bioinformatics analysis showed the predicted binding sequence of RFC2 3′-UTR. (B) Dual luciferase assay was performed in cells co-transfected with WT RFC2 plasmid or MUT RFC2 plasmid and miR-NC or miR-744-5p mimic in U251 and U87 cells. **P<0.001, one-way ANOVA with Tukey's test. (C) Expression of miR-744-5p in GBM tumor tissues (n=39) and adjacent controls (n=39) from patients with GBM was analyzed by RT-qPCR. **P<0.001, compared with Normal group using paired Student's t-test. (D) Correlation between RFC2 and miR-744-5p expression in GBM tissues. (E) RT-qPCR detection of RFC2 expression in NHA, U251 and U87 cells. *P<0.05 and **P<0.001 compared with NHA using one-way ANOVA with Dunnett's test. (F) RT-qPCR analysis of the mRNA expression of RFC2 in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, si-RFC2, and Si-RFC2+ miR-744-5p inhibitor. (G) Western blot analysis of RFC2 protein expression in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, si-RFC2, and si-RFC2+ miR-744-5p inhibitor. (F-G) CON, blank control; NC, negative control. **P<0.001 compared with CON using one-way ANOVA with Dunnett's test. RFC2, replication factor C subunit 2; GBM, glioblastoma; RT-q, reverse transcription-quantitative; si(RNA), small interfering; OE, overexpression; NC, negative control; WT, wild-type; MUT, mutant; miR, microRNA.

Journal: Oncology Letters

Article Title: MicroRNA-744-5p inhibits glioblastoma malignancy by suppressing replication factor C subunit 2

doi: 10.3892/ol.2021.12869

Figure Lengend Snippet: RFC2 is a direct target of miR-744-5p in GBM. (A) Bioinformatics analysis showed the predicted binding sequence of RFC2 3′-UTR. (B) Dual luciferase assay was performed in cells co-transfected with WT RFC2 plasmid or MUT RFC2 plasmid and miR-NC or miR-744-5p mimic in U251 and U87 cells. **P<0.001, one-way ANOVA with Tukey's test. (C) Expression of miR-744-5p in GBM tumor tissues (n=39) and adjacent controls (n=39) from patients with GBM was analyzed by RT-qPCR. **P<0.001, compared with Normal group using paired Student's t-test. (D) Correlation between RFC2 and miR-744-5p expression in GBM tissues. (E) RT-qPCR detection of RFC2 expression in NHA, U251 and U87 cells. *P<0.05 and **P<0.001 compared with NHA using one-way ANOVA with Dunnett's test. (F) RT-qPCR analysis of the mRNA expression of RFC2 in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, si-RFC2, and Si-RFC2+ miR-744-5p inhibitor. (G) Western blot analysis of RFC2 protein expression in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, si-RFC2, and si-RFC2+ miR-744-5p inhibitor. (F-G) CON, blank control; NC, negative control. **P<0.001 compared with CON using one-way ANOVA with Dunnett's test. RFC2, replication factor C subunit 2; GBM, glioblastoma; RT-q, reverse transcription-quantitative; si(RNA), small interfering; OE, overexpression; NC, negative control; WT, wild-type; MUT, mutant; miR, microRNA.

Article Snippet: The human GBM cell lines, U87 (cat. no. HTB-14; GBM of unknown origin) and A172 (cat. no. CRL-1620) were purchased from the American Type Culture Collection.

Techniques: Binding Assay, Sequencing, Luciferase, Transfection, Plasmid Preparation, Expressing, Quantitative RT-PCR, Western Blot, Control, Negative Control, Reverse Transcription, Over Expression, Mutagenesis

miR-744-5p targeting to RFC2 suppresses glioblastoma progression. (A) Viability of U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor was determined by Cell Counting Kit 8 analysis. (B) Proliferation was detected in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor by BrdU assay. (C) Wound-healing assay was performed in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor. (D) Adhesion ability was detected in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor. (E) Caspase-3 activity was determined in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor by caspase-3 activity assay kit. (F) Protein expression levels of Bax and Bcl-2 were determined in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor by western blot assay. *P<0.05 and **P<0.001, compared with CON using one-way ANOVA with Dunnett's test. CON, blank control; NC, negative control; Si-RFC2, SiRNA-RFC2; Si-RFC2+ miR-744-5p inhibitor, SiRNA-RFC2+ miR-744-5p inhibitor; RFC2, replication factor C subunit 2.

Journal: Oncology Letters

Article Title: MicroRNA-744-5p inhibits glioblastoma malignancy by suppressing replication factor C subunit 2

doi: 10.3892/ol.2021.12869

Figure Lengend Snippet: miR-744-5p targeting to RFC2 suppresses glioblastoma progression. (A) Viability of U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor was determined by Cell Counting Kit 8 analysis. (B) Proliferation was detected in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor by BrdU assay. (C) Wound-healing assay was performed in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor. (D) Adhesion ability was detected in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor. (E) Caspase-3 activity was determined in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor by caspase-3 activity assay kit. (F) Protein expression levels of Bax and Bcl-2 were determined in U251 and U87 cells transfected with NC, miR-744-5p inhibitor, Si-RFC2, and Si-RFC2+ miR-744-5p inhibitor by western blot assay. *P<0.05 and **P<0.001, compared with CON using one-way ANOVA with Dunnett's test. CON, blank control; NC, negative control; Si-RFC2, SiRNA-RFC2; Si-RFC2+ miR-744-5p inhibitor, SiRNA-RFC2+ miR-744-5p inhibitor; RFC2, replication factor C subunit 2.

Article Snippet: The human GBM cell lines, U87 (cat. no. HTB-14; GBM of unknown origin) and A172 (cat. no. CRL-1620) were purchased from the American Type Culture Collection.

Techniques: Transfection, Cell Counting, BrdU Staining, Wound Healing Assay, Activity Assay, Caspase-3 Activity Assay, Expressing, Western Blot, Control, Negative Control

$lncRNA DDX11-AS1 expression is upregulated in human glioma specimens. ( A ) Expression of lncRNA DDX11-AS1 was evaluated in 32 glioma tissues and 12 normal brain tissues by RT-qPCR. ( B ) Expression of lncRNA DDX11-AS1 was identified in 9 low-grade glioma (LGG) tissues and 23 glioblastoma (GBM) tissues by RT-qPCR. ( C ) lncRNA DDX11-AS1 expression level in open-access datasets of TCGA and GTEx ( n = 1152 for normal brain tissues and n = 689 for glioblastoma). ( D ) Kaplan-Meier plots of overall survival in glioma patients with high ( n = 337) and low ( n = 336) levels of DDX11-AS1 in the TCGA database. ( E ) Kaplan-Meier plots of overall survival in glioma patients with high ( n = 113) and low ( n = 109) levels of DDX11-AS1 in the CGGA database. ( F ) Expression of lncRNA DDX11-AS1 in HEB cells and four glioma cell lines ( n = 6). ( G , H ) Levels of DDX11-AS1 in the nuclear and cytoplasmic fractions of U87 and U251 cells ( n = 6). Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test$

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: lncRNA DDX11-AS1 expression is upregulated in human glioma specimens. ( A ) Expression of lncRNA DDX11-AS1 was evaluated in 32 glioma tissues and 12 normal brain tissues by RT-qPCR. ( B ) Expression of lncRNA DDX11-AS1 was identified in 9 low-grade glioma (LGG) tissues and 23 glioblastoma (GBM) tissues by RT-qPCR. ( C ) lncRNA DDX11-AS1 expression level in open-access datasets of TCGA and GTEx ( n = 1152 for normal brain tissues and n = 689 for glioblastoma). ( D ) Kaplan-Meier plots of overall survival in glioma patients with high ( n = 337) and low ( n = 336) levels of DDX11-AS1 in the TCGA database. ( E ) Kaplan-Meier plots of overall survival in glioma patients with high ( n = 113) and low ( n = 109) levels of DDX11-AS1 in the CGGA database. ( F ) Expression of lncRNA DDX11-AS1 in HEB cells and four glioma cell lines ( n = 6). ( G , H ) Levels of DDX11-AS1 in the nuclear and cytoplasmic fractions of U87 and U251 cells ( n = 6). Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Article Snippet: Human glioma cell lines U87 MG (ATCC; glioblastoma of unknown origin; catalog #TCHu138; National Collection of Authenticated Cell Cultures, Shanghai, China), U251 MG (catalog #TCHu58; National Collection of Authenticated Cell Cultures), T98G (catalog #ORC0333; ORiCells Biotechnology, Shanghai, China) and U373 MG (catalog #YC-A085; UBIGENE, Guangzhou, China) were used.

Techniques: Expressing, Quantitative RT-PCR

Knockdown of DDX11-AS1 suppresses the proliferation and migration in glioma cells. Glioma cells transfected with shDDX11-AS1 or sh-NC were used. ( A ) Expression level of lncRNA DDX11-AS1 in glioma cells. The expression level of sh-DDX11-AS1 U87 and U251 is normalized to GAPDH , and expressed as fold change over the sh-NC U87 or sh-NC U251 group, respectively ( n = 6). ( B , C ) CCK-8 assay of ( B ) U87 and ( C ) U251 cells ( n = 6). ( D , E ) Colony formation assay of ( D ) U87 and ( E ) U251 cells ( n = 6). ( F , G ) Representative images of scratch wound healing assay of ( F ) U87 and ( G ) U251 cells. ( H ) The percentage of wound closure at 24 h ( n = 6). ( I ) Transwell assay of U87 and U251 cells. ( J ) Quantified data depicting migrated cell number ( n = 6). Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: Knockdown of DDX11-AS1 suppresses the proliferation and migration in glioma cells. Glioma cells transfected with shDDX11-AS1 or sh-NC were used. ( A ) Expression level of lncRNA DDX11-AS1 in glioma cells. The expression level of sh-DDX11-AS1 U87 and U251 is normalized to GAPDH , and expressed as fold change over the sh-NC U87 or sh-NC U251 group, respectively ( n = 6). ( B , C ) CCK-8 assay of ( B ) U87 and ( C ) U251 cells ( n = 6). ( D , E ) Colony formation assay of ( D ) U87 and ( E ) U251 cells ( n = 6). ( F , G ) Representative images of scratch wound healing assay of ( F ) U87 and ( G ) U251 cells. ( H ) The percentage of wound closure at 24 h ( n = 6). ( I ) Transwell assay of U87 and U251 cells. ( J ) Quantified data depicting migrated cell number ( n = 6). Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Techniques: Knockdown, Migration, Transfection, Expressing, CCK-8 Assay, Colony Assay, Wound Healing Assay, Transwell Assay

Overexpression of DDX11-AS1 promotes the proliferation and migration in glioma cells. Glioma cells with DDX11-AS1 overexpression or harboring the empty vector were used. ( A ) Expression level of lncRNA DDX11-AS1 in glioma cells. The expression level of oe-DDX11-AS1 U87 and U251 is normalized to GAPDH , and expressed as fold change over the oe-NC U87 or oe-NC U251 group, respectively ( n = 6). ( B , C ) CCK-8 assay of ( B ) U87 and ( C ) U251 cells ( n = 6). ( D , E ) Colony formation assay of ( D ) U87 and ( E ) U251 cells ( n = 6). ( F , G ) Representative scratch assay images of ( F ) U87 and ( G ) U251 cells. ( H ) The percentage of wound closure at 24 h ( n = 6). ( I ) Transwell migration analysis of U87 and U251 cells. ( J ) Quantified data depicting migrated cell number ( n = 6). Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: Overexpression of DDX11-AS1 promotes the proliferation and migration in glioma cells. Glioma cells with DDX11-AS1 overexpression or harboring the empty vector were used. ( A ) Expression level of lncRNA DDX11-AS1 in glioma cells. The expression level of oe-DDX11-AS1 U87 and U251 is normalized to GAPDH , and expressed as fold change over the oe-NC U87 or oe-NC U251 group, respectively ( n = 6). ( B , C ) CCK-8 assay of ( B ) U87 and ( C ) U251 cells ( n = 6). ( D , E ) Colony formation assay of ( D ) U87 and ( E ) U251 cells ( n = 6). ( F , G ) Representative scratch assay images of ( F ) U87 and ( G ) U251 cells. ( H ) The percentage of wound closure at 24 h ( n = 6). ( I ) Transwell migration analysis of U87 and U251 cells. ( J ) Quantified data depicting migrated cell number ( n = 6). Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Techniques: Over Expression, Migration, Plasmid Preparation, Expressing, CCK-8 Assay, Colony Assay, Wound Healing Assay

DDX11-AS1 competitively binds miR-1183 through competing endogenous RNA (ceRNA) mechanism. ( A ) In silico analysis of the binding site of miR-1183 within DDX11-AS1 sequence. ( B ) Correlation between DDX11-AS1 and miR-1183 expression in clinical glioma samples ( n = 32). ( C , D ) The expression level of miR-1183 in glioma cells with DDX11-AS1 ( C ) knockdown or ( D ) overexpression ( n = 6). ( E ) The relative luciferase activity was examined in U87 glioma cells co-transfected with DDX11-AS1 wild-type (WT) or DDX11-AS1 mutant (MUT) and miR-1183 mimics or the miR-NC. ( F , G ) RIP assay in ( F ) U87 and ( G ) U251 glioma cells. ( H ) Binding of miR-1183 and miR-NC to DDX11-AS1 in the RNA pull-down assay (GAPDH as control). ( I ) RNA FISH for DDX11-AS1 and miR-1183 in human glioma sample. Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: DDX11-AS1 competitively binds miR-1183 through competing endogenous RNA (ceRNA) mechanism. ( A ) In silico analysis of the binding site of miR-1183 within DDX11-AS1 sequence. ( B ) Correlation between DDX11-AS1 and miR-1183 expression in clinical glioma samples ( n = 32). ( C , D ) The expression level of miR-1183 in glioma cells with DDX11-AS1 ( C ) knockdown or ( D ) overexpression ( n = 6). ( E ) The relative luciferase activity was examined in U87 glioma cells co-transfected with DDX11-AS1 wild-type (WT) or DDX11-AS1 mutant (MUT) and miR-1183 mimics or the miR-NC. ( F , G ) RIP assay in ( F ) U87 and ( G ) U251 glioma cells. ( H ) Binding of miR-1183 and miR-NC to DDX11-AS1 in the RNA pull-down assay (GAPDH as control). ( I ) RNA FISH for DDX11-AS1 and miR-1183 in human glioma sample. Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Techniques: In Silico, Binding Assay, Sequencing, Expressing, Knockdown, Over Expression, Luciferase, Activity Assay, Transfection, Mutagenesis, Pull Down Assay, Control

DDX11-AS1 promotes glioma cell proliferation and migration by targeting miR-1183. Glioma cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed by miR-1183 inhibitor treatment were used. ( A , B ) CCK-8 assays of ( A ) U87 and ( B ) U251 glioma cells ( n = 6). ( C , D ) Colony formation assays of ( C ) U87 and ( D ) U251 glioma cells ( n = 6). ( E ) Scratch wound healing assay of U87 and U251 glioma cells. ( F ) Transwell assay of U87 and U251 glioma cells. The right panel is the quantified data depicting migrated cell number ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: DDX11-AS1 promotes glioma cell proliferation and migration by targeting miR-1183. Glioma cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed by miR-1183 inhibitor treatment were used. ( A , B ) CCK-8 assays of ( A ) U87 and ( B ) U251 glioma cells ( n = 6). ( C , D ) Colony formation assays of ( C ) U87 and ( D ) U251 glioma cells ( n = 6). ( E ) Scratch wound healing assay of U87 and U251 glioma cells. ( F ) Transwell assay of U87 and U251 glioma cells. The right panel is the quantified data depicting migrated cell number ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Techniques: Migration, Transfection, CCK-8 Assay, Wound Healing Assay, Transwell Assay

E2F7 is a target of miR-1183. ( A ) The bioinformatics analysis tools were used to predict the binding site of miR-1183 in E2F7. ( B ) Correlation between miR-1183 and E2F7 expression. ( C ) Luciferase activity in U87 cells co-transfected with miR-1183 and WT/MUT E2F7 reporter constructs ( n = 6). ( D – G ) U87 and U251 cells transfected with miR-1183, miR-NC or E2F7-overexpression vectors were used; ( D , E ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6); ( F , G ) CCK-8 assay of ( F ) U87 and ( G ) U251 cells ( n = 6); ( H , I ) U87 and U251 cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed with miR-1183 inhibitor treatment were used. ( H ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6). ( I ) Immunoblotting assays detected E2F7 and GAPDH in U87 and U251 cells. The bar chart quantifies relative E2F7 protein abundance normalized to GAPDH ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: E2F7 is a target of miR-1183. ( A ) The bioinformatics analysis tools were used to predict the binding site of miR-1183 in E2F7. ( B ) Correlation between miR-1183 and E2F7 expression. ( C ) Luciferase activity in U87 cells co-transfected with miR-1183 and WT/MUT E2F7 reporter constructs ( n = 6). ( D – G ) U87 and U251 cells transfected with miR-1183, miR-NC or E2F7-overexpression vectors were used; ( D , E ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6); ( F , G ) CCK-8 assay of ( F ) U87 and ( G ) U251 cells ( n = 6); ( H , I ) U87 and U251 cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed with miR-1183 inhibitor treatment were used. ( H ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6). ( I ) Immunoblotting assays detected E2F7 and GAPDH in U87 and U251 cells. The bar chart quantifies relative E2F7 protein abundance normalized to GAPDH ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Techniques: Binding Assay, Expressing, Luciferase, Activity Assay, Transfection, Construct, Over Expression, Quantitative RT-PCR, CCK-8 Assay, Western Blot, Quantitative Proteomics

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