unknown origin u87 Search Results


u87  (ATCC)
99
ATCC u87
Effect of 3α-THP on human GB cell migration. ( a ) Representative images of the scratch area from U251 cells treated with vehicle (V, ethanol 0.1% in the medium), progesterone (P4; 10 nM), or allopregnanolone (3α-THP; 10, 100 nM and 1 µM). Percentage migration graphs of ( b ) U251, ( c ) <t>U87,</t> and ( d ) LN229 human GB cell lines. Each point represents the mean ± SEM. U251 (Graph b): # p < 0.05 for P4 and 3α-THP 100 nM vs. V; * p < 0.05 for P4 and all concentrations of 3α-THP vs. V. U87 (Graph c): * p < 0.05 for 3α-THP 10 nM, 100 nM and 1 µM vs. V. LN229 (Graph d): + p < 0.05 3α-THP 10 nM and 1 µM vs. V; * p < 0.05 for 3α-THP 100 nM vs. all other treatments. n = 3 for U251 and U87 cells; n = 4 for LN229 cell line.
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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99
ATCC human glioma cell lines u 87mg
Effect of 3α-THP on human GB cell migration. ( a ) Representative images of the scratch area from U251 cells treated with vehicle (V, ethanol 0.1% in the medium), progesterone (P4; 10 nM), or allopregnanolone (3α-THP; 10, 100 nM and 1 µM). Percentage migration graphs of ( b ) U251, ( c ) <t>U87,</t> and ( d ) LN229 human GB cell lines. Each point represents the mean ± SEM. U251 (Graph b): # p < 0.05 for P4 and 3α-THP 100 nM vs. V; * p < 0.05 for P4 and all concentrations of 3α-THP vs. V. U87 (Graph c): * p < 0.05 for 3α-THP 10 nM, 100 nM and 1 µM vs. V. LN229 (Graph d): + p < 0.05 3α-THP 10 nM and 1 µM vs. V; * p < 0.05 for 3α-THP 100 nM vs. all other treatments. n = 3 for U251 and U87 cells; n = 4 for LN229 cell line.
Human Glioma Cell Lines U 87mg, 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
https://www.bioz.com/product/unknown+origin+u87/U-87+MG/pmc06579993-21-0-5
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97
ATCC u 87 mg atcc htb 14 glio blastoma
Effect of 3α-THP on human GB cell migration. ( a ) Representative images of the scratch area from U251 cells treated with vehicle (V, ethanol 0.1% in the medium), progesterone (P4; 10 nM), or allopregnanolone (3α-THP; 10, 100 nM and 1 µM). Percentage migration graphs of ( b ) U251, ( c ) <t>U87,</t> and ( d ) LN229 human GB cell lines. Each point represents the mean ± SEM. U251 (Graph b): # p < 0.05 for P4 and 3α-THP 100 nM vs. V; * p < 0.05 for P4 and all concentrations of 3α-THP vs. V. U87 (Graph c): * p < 0.05 for 3α-THP 10 nM, 100 nM and 1 µM vs. V. LN229 (Graph d): + p < 0.05 3α-THP 10 nM and 1 µM vs. V; * p < 0.05 for 3α-THP 100 nM vs. all other treatments. n = 3 for U251 and U87 cells; n = 4 for LN229 cell line.
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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86
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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97
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
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Image Search Results


Effect of 3α-THP on human GB cell migration. ( a ) Representative images of the scratch area from U251 cells treated with vehicle (V, ethanol 0.1% in the medium), progesterone (P4; 10 nM), or allopregnanolone (3α-THP; 10, 100 nM and 1 µM). Percentage migration graphs of ( b ) U251, ( c ) U87, and ( d ) LN229 human GB cell lines. Each point represents the mean ± SEM. U251 (Graph b): # p < 0.05 for P4 and 3α-THP 100 nM vs. V; * p < 0.05 for P4 and all concentrations of 3α-THP vs. V. U87 (Graph c): * p < 0.05 for 3α-THP 10 nM, 100 nM and 1 µM vs. V. LN229 (Graph d): + p < 0.05 3α-THP 10 nM and 1 µM vs. V; * p < 0.05 for 3α-THP 100 nM vs. all other treatments. n = 3 for U251 and U87 cells; n = 4 for LN229 cell line.

Journal: International Journal of Molecular Sciences

Article Title: Allopregnanolone Promotes Migration and Invasion of Human Glioblastoma Cells through the Protein Tyrosine Kinase c-Src Activation

doi: 10.3390/ijms23094996

Figure Lengend Snippet: Effect of 3α-THP on human GB cell migration. ( a ) Representative images of the scratch area from U251 cells treated with vehicle (V, ethanol 0.1% in the medium), progesterone (P4; 10 nM), or allopregnanolone (3α-THP; 10, 100 nM and 1 µM). Percentage migration graphs of ( b ) U251, ( c ) U87, and ( d ) LN229 human GB cell lines. Each point represents the mean ± SEM. U251 (Graph b): # p < 0.05 for P4 and 3α-THP 100 nM vs. V; * p < 0.05 for P4 and all concentrations of 3α-THP vs. V. U87 (Graph c): * p < 0.05 for 3α-THP 10 nM, 100 nM and 1 µM vs. V. LN229 (Graph d): + p < 0.05 3α-THP 10 nM and 1 µM vs. V; * p < 0.05 for 3α-THP 100 nM vs. all other treatments. n = 3 for U251 and U87 cells; n = 4 for LN229 cell line.

Article Snippet: Human GB cell lines U251, LN229, T98G, and U87 (unknown origin) were purchased from ATCC.

Techniques: Migration

Effect of 3α-THP on the invasion of human GB cell lines. Cells were treated with vehicle (V; ethanol, 0.1% in the medium), P4 (10 nM), and 3α-THP (100 nM) for 24 h. Representative images of ( a ) U251; ( c ) U87, and ( e ) LN229 invasion assays. All photographs were taken at 10× augment. Graphs of the invading cells number per field: ( b ) U251; ( d ) U87; and ( f ) LN229 cell lines. Each column represents the mean ± SEM. n = 3 for all cell lines evaluated; * p < 0.05 vs. V.

Journal: International Journal of Molecular Sciences

Article Title: Allopregnanolone Promotes Migration and Invasion of Human Glioblastoma Cells through the Protein Tyrosine Kinase c-Src Activation

doi: 10.3390/ijms23094996

Figure Lengend Snippet: Effect of 3α-THP on the invasion of human GB cell lines. Cells were treated with vehicle (V; ethanol, 0.1% in the medium), P4 (10 nM), and 3α-THP (100 nM) for 24 h. Representative images of ( a ) U251; ( c ) U87, and ( e ) LN229 invasion assays. All photographs were taken at 10× augment. Graphs of the invading cells number per field: ( b ) U251; ( d ) U87; and ( f ) LN229 cell lines. Each column represents the mean ± SEM. n = 3 for all cell lines evaluated; * p < 0.05 vs. V.

Article Snippet: Human GB cell lines U251, LN229, T98G, and U87 (unknown origin) were purchased from ATCC.

Techniques:

AKR1C1-4 are differentially expressed in GB cells. The expression of AKR1C1-4 was detected in a total protein extract from normal human astrocytes (HA) and different human GB cell lines. ( a ) Representative Western blots of AKR1C1-4 and α-Tubulin, which was used as a loading control. ( b ) Densitometric analysis graph. Each column represents the mean ± SEM. n = 3; * p < 0.05 U251, T98G, and LN229 vs. HA and U87 cell lines.

Journal: International Journal of Molecular Sciences

Article Title: Allopregnanolone Promotes Migration and Invasion of Human Glioblastoma Cells through the Protein Tyrosine Kinase c-Src Activation

doi: 10.3390/ijms23094996

Figure Lengend Snippet: AKR1C1-4 are differentially expressed in GB cells. The expression of AKR1C1-4 was detected in a total protein extract from normal human astrocytes (HA) and different human GB cell lines. ( a ) Representative Western blots of AKR1C1-4 and α-Tubulin, which was used as a loading control. ( b ) Densitometric analysis graph. Each column represents the mean ± SEM. n = 3; * p < 0.05 U251, T98G, and LN229 vs. HA and U87 cell lines.

Article Snippet: Human GB cell lines U251, LN229, T98G, and U87 (unknown origin) were purchased from ATCC.

Techniques: Expressing, Western Blot, Control

Effect of 3α-THP and the pharmacological inhibitor of c-SRC PP2 on U251 and U87 cell invasion. ( a ) Representative images of U251 cell invasion assays. All photographs were taken at 10× augment. ( b ) Graph of the number of invading U251 cells per field. Each column represents the mean ± SEM., n = 4; * p < 0.05 3α-THP vs. V (EtOH, and DMSO); ** p < 0.005 3α-THP vs. 3α-THP + PP2. ( c ) Graph of the number of invading U87 cells per field. Each column represents the mean ± SEM., n = 4; * p < 0.05 3α-THP vs. all other treatments.

Journal: International Journal of Molecular Sciences

Article Title: Allopregnanolone Promotes Migration and Invasion of Human Glioblastoma Cells through the Protein Tyrosine Kinase c-Src Activation

doi: 10.3390/ijms23094996

Figure Lengend Snippet: Effect of 3α-THP and the pharmacological inhibitor of c-SRC PP2 on U251 and U87 cell invasion. ( a ) Representative images of U251 cell invasion assays. All photographs were taken at 10× augment. ( b ) Graph of the number of invading U251 cells per field. Each column represents the mean ± SEM., n = 4; * p < 0.05 3α-THP vs. V (EtOH, and DMSO); ** p < 0.005 3α-THP vs. 3α-THP + PP2. ( c ) Graph of the number of invading U87 cells per field. Each column represents the mean ± SEM., n = 4; * p < 0.05 3α-THP vs. all other treatments.

Article Snippet: Human GB cell lines U251, LN229, T98G, and U87 (unknown origin) were purchased from ATCC.

Techniques:

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

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: 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

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: 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

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: 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)

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: 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)

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