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Genechem plasmids engineered to overexpress igf2
Development of a prognostic model associated with glycolysis-related gene subtypes. ( A ) The C-index of 85 machine-learning algorithm combinations was calculated in the ICGC and TCGA databases. ( B ) An importance assessment was conducted for genes within the model. ( C ) Kaplan–Meier survival analysis compared OS between groups with high and low <t>IGF2</t> expression. ( D ) GSEA revealed IGF2’s association with glycolysis. ( E , F ) GSEA enrichment analysis was performed for both the high-expression and low-expression IGF2 groups
Plasmids Engineered To Overexpress Igf2, supplied by Genechem, 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/plasmids+engineered+to+overexpress+igf2/sirna+constructs+igf2bp2/pmc11292870-123-4-8
Average 90 stars, based on 1 article reviews
plasmids engineered to overexpress igf2 - by Bioz Stars, 2026-09
90/100 stars

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Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes

Journal: BMC Cancer

doi: 10.1186/s12885-024-12688-7

Development of a prognostic model associated with glycolysis-related gene subtypes. ( A ) The C-index of 85 machine-learning algorithm combinations was calculated in the ICGC and TCGA databases. ( B ) An importance assessment was conducted for genes within the model. ( C ) Kaplan–Meier survival analysis compared OS between groups with high and low IGF2 expression. ( D ) GSEA revealed IGF2’s association with glycolysis. ( E , F ) GSEA enrichment analysis was performed for both the high-expression and low-expression IGF2 groups
Figure Legend Snippet: Development of a prognostic model associated with glycolysis-related gene subtypes. ( A ) The C-index of 85 machine-learning algorithm combinations was calculated in the ICGC and TCGA databases. ( B ) An importance assessment was conducted for genes within the model. ( C ) Kaplan–Meier survival analysis compared OS between groups with high and low IGF2 expression. ( D ) GSEA revealed IGF2’s association with glycolysis. ( E , F ) GSEA enrichment analysis was performed for both the high-expression and low-expression IGF2 groups

Techniques Used: Expressing

IGF2 promoted OC cell proliferation, migration, and invasion, and the resistance to cisplatin. ( A ) IGF2 expression in normal ovarian tissues, benign, borderline epithelial tumors, and EOC detected by IHC assay (ns, not significant; * p < 0.05; ** p < 0.01,*** p < 0.001, **** p < 0.0001 in t-test. N = 5). ( B ) qRT-PCR analysis of IGF2 expression. ( C ) Western blot analysis of IGF2 expression. Protein expression levels were quantified by grey analysis (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( D ) EdU assays demonstrated the cell proliferation ability upon reduction of IGF2 expression (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( E ) Wound healing assays showed the migration ability of SKOV-3 and A2780 cell lines treated with si-IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( F ) Transwell invasion assays showed the invasion ability of SKOV3 and A2780 cell lines treated with si-IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( G ) CCK-8 assays displayed the sensitivity of OC cells to cisplatin treatment following IGF2 knockdown (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3)
Figure Legend Snippet: IGF2 promoted OC cell proliferation, migration, and invasion, and the resistance to cisplatin. ( A ) IGF2 expression in normal ovarian tissues, benign, borderline epithelial tumors, and EOC detected by IHC assay (ns, not significant; * p < 0.05; ** p < 0.01,*** p < 0.001, **** p < 0.0001 in t-test. N = 5). ( B ) qRT-PCR analysis of IGF2 expression. ( C ) Western blot analysis of IGF2 expression. Protein expression levels were quantified by grey analysis (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( D ) EdU assays demonstrated the cell proliferation ability upon reduction of IGF2 expression (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( E ) Wound healing assays showed the migration ability of SKOV-3 and A2780 cell lines treated with si-IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( F ) Transwell invasion assays showed the invasion ability of SKOV3 and A2780 cell lines treated with si-IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( G ) CCK-8 assays displayed the sensitivity of OC cells to cisplatin treatment following IGF2 knockdown (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3)

Techniques Used: Migration, Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Knockdown

Relationships between  IGF2  expression and clinicopathological parameters in EOC patients
Figure Legend Snippet: Relationships between IGF2 expression and clinicopathological parameters in EOC patients

Techniques Used: Expressing

IGF2 promoted the glycolysis pathway. ( A ) Glucose uptake experiments demonstrated the glucose uptake ability of OC cells after knockdown IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( B ) Lactate production experiments indicated that IGF2 inhibition influenced lactate content generated by OC cells (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( C ) Western blot analysis of glycolysis enzymes (including HK2, PKM2, ENO1, PGK1, LDHA) in IGF2-knockdown cells (The blot has been cropped, and the original blot is shown in supplementary material .) (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( D ) Edu assay analysis revealed changes in the proliferation of OC cells with either vector control or IGF2 overexpression, treated with or without the glycolysis inhibitor 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( E ) The wound healing assay detected migration capability in vector control or IGF2-overexpressing cells, cultured with or without 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( F ) The transwell assay indicated the invasion capability of OC cells upon vector control or IGF2 overexpression, cultured with or without 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3)
Figure Legend Snippet: IGF2 promoted the glycolysis pathway. ( A ) Glucose uptake experiments demonstrated the glucose uptake ability of OC cells after knockdown IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( B ) Lactate production experiments indicated that IGF2 inhibition influenced lactate content generated by OC cells (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( C ) Western blot analysis of glycolysis enzymes (including HK2, PKM2, ENO1, PGK1, LDHA) in IGF2-knockdown cells (The blot has been cropped, and the original blot is shown in supplementary material .) (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( D ) Edu assay analysis revealed changes in the proliferation of OC cells with either vector control or IGF2 overexpression, treated with or without the glycolysis inhibitor 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( E ) The wound healing assay detected migration capability in vector control or IGF2-overexpressing cells, cultured with or without 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( F ) The transwell assay indicated the invasion capability of OC cells upon vector control or IGF2 overexpression, cultured with or without 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3)

Techniques Used: Knockdown, Inhibition, Generated, Western Blot, EdU Assay, Plasmid Preparation, Control, Over Expression, Wound Healing Assay, Migration, Cell Culture, Transwell Assay

Related Articles

Expressing:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Migration:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Quantitative RT-PCR:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Western Blot:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

CCK-8 Assay:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Knockdown:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Inhibition:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Generated:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

EdU Assay:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Plasmid Preparation:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Control:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Over Expression:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Wound Healing Assay:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Cell Culture:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Transwell Assay:

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes
Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).



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Genechem plasmids engineered to overexpress igf2
Development of a prognostic model associated with glycolysis-related gene subtypes. ( A ) The C-index of 85 machine-learning algorithm combinations was calculated in the ICGC and TCGA databases. ( B ) An importance assessment was conducted for genes within the model. ( C ) Kaplan–Meier survival analysis compared OS between groups with high and low <t>IGF2</t> expression. ( D ) GSEA revealed IGF2’s association with glycolysis. ( E , F ) GSEA enrichment analysis was performed for both the high-expression and low-expression IGF2 groups
Plasmids Engineered To Overexpress Igf2, supplied by Genechem, 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/plasmids+engineered+to+overexpress+igf2/sirna+constructs+igf2bp2/pmc11292870-123-4-8
Average 90 stars, based on 1 article reviews
plasmids engineered to overexpress igf2 - by Bioz Stars, 2026-09
90/100 stars
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Development of a prognostic model associated with glycolysis-related gene subtypes. ( A ) The C-index of 85 machine-learning algorithm combinations was calculated in the ICGC and TCGA databases. ( B ) An importance assessment was conducted for genes within the model. ( C ) Kaplan–Meier survival analysis compared OS between groups with high and low IGF2 expression. ( D ) GSEA revealed IGF2’s association with glycolysis. ( E , F ) GSEA enrichment analysis was performed for both the high-expression and low-expression IGF2 groups

Journal: BMC Cancer

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes

doi: 10.1186/s12885-024-12688-7

Figure Lengend Snippet: Development of a prognostic model associated with glycolysis-related gene subtypes. ( A ) The C-index of 85 machine-learning algorithm combinations was calculated in the ICGC and TCGA databases. ( B ) An importance assessment was conducted for genes within the model. ( C ) Kaplan–Meier survival analysis compared OS between groups with high and low IGF2 expression. ( D ) GSEA revealed IGF2’s association with glycolysis. ( E , F ) GSEA enrichment analysis was performed for both the high-expression and low-expression IGF2 groups

Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Techniques: Expressing

IGF2 promoted OC cell proliferation, migration, and invasion, and the resistance to cisplatin. ( A ) IGF2 expression in normal ovarian tissues, benign, borderline epithelial tumors, and EOC detected by IHC assay (ns, not significant; * p < 0.05; ** p < 0.01,*** p < 0.001, **** p < 0.0001 in t-test. N = 5). ( B ) qRT-PCR analysis of IGF2 expression. ( C ) Western blot analysis of IGF2 expression. Protein expression levels were quantified by grey analysis (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( D ) EdU assays demonstrated the cell proliferation ability upon reduction of IGF2 expression (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( E ) Wound healing assays showed the migration ability of SKOV-3 and A2780 cell lines treated with si-IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( F ) Transwell invasion assays showed the invasion ability of SKOV3 and A2780 cell lines treated with si-IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( G ) CCK-8 assays displayed the sensitivity of OC cells to cisplatin treatment following IGF2 knockdown (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3)

Journal: BMC Cancer

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes

doi: 10.1186/s12885-024-12688-7

Figure Lengend Snippet: IGF2 promoted OC cell proliferation, migration, and invasion, and the resistance to cisplatin. ( A ) IGF2 expression in normal ovarian tissues, benign, borderline epithelial tumors, and EOC detected by IHC assay (ns, not significant; * p < 0.05; ** p < 0.01,*** p < 0.001, **** p < 0.0001 in t-test. N = 5). ( B ) qRT-PCR analysis of IGF2 expression. ( C ) Western blot analysis of IGF2 expression. Protein expression levels were quantified by grey analysis (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( D ) EdU assays demonstrated the cell proliferation ability upon reduction of IGF2 expression (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( E ) Wound healing assays showed the migration ability of SKOV-3 and A2780 cell lines treated with si-IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( F ) Transwell invasion assays showed the invasion ability of SKOV3 and A2780 cell lines treated with si-IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( G ) CCK-8 assays displayed the sensitivity of OC cells to cisplatin treatment following IGF2 knockdown (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3)

Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Techniques: Migration, Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Knockdown

Relationships between  IGF2  expression and clinicopathological parameters in EOC patients

Journal: BMC Cancer

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes

doi: 10.1186/s12885-024-12688-7

Figure Lengend Snippet: Relationships between IGF2 expression and clinicopathological parameters in EOC patients

Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Techniques: Expressing

IGF2 promoted the glycolysis pathway. ( A ) Glucose uptake experiments demonstrated the glucose uptake ability of OC cells after knockdown IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( B ) Lactate production experiments indicated that IGF2 inhibition influenced lactate content generated by OC cells (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( C ) Western blot analysis of glycolysis enzymes (including HK2, PKM2, ENO1, PGK1, LDHA) in IGF2-knockdown cells (The blot has been cropped, and the original blot is shown in supplementary material .) (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( D ) Edu assay analysis revealed changes in the proliferation of OC cells with either vector control or IGF2 overexpression, treated with or without the glycolysis inhibitor 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( E ) The wound healing assay detected migration capability in vector control or IGF2-overexpressing cells, cultured with or without 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( F ) The transwell assay indicated the invasion capability of OC cells upon vector control or IGF2 overexpression, cultured with or without 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3)

Journal: BMC Cancer

Article Title: Single-cell transcriptome analysis revealed heterogeneity in glycolysis and identified IGF2 as a therapeutic target for ovarian cancer subtypes

doi: 10.1186/s12885-024-12688-7

Figure Lengend Snippet: IGF2 promoted the glycolysis pathway. ( A ) Glucose uptake experiments demonstrated the glucose uptake ability of OC cells after knockdown IGF2 (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( B ) Lactate production experiments indicated that IGF2 inhibition influenced lactate content generated by OC cells (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( C ) Western blot analysis of glycolysis enzymes (including HK2, PKM2, ENO1, PGK1, LDHA) in IGF2-knockdown cells (The blot has been cropped, and the original blot is shown in supplementary material .) (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( D ) Edu assay analysis revealed changes in the proliferation of OC cells with either vector control or IGF2 overexpression, treated with or without the glycolysis inhibitor 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( E ) The wound healing assay detected migration capability in vector control or IGF2-overexpressing cells, cultured with or without 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3). ( F ) The transwell assay indicated the invasion capability of OC cells upon vector control or IGF2 overexpression, cultured with or without 2-DG. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 in t-test. N = 3)

Article Snippet: Plasmids engineered to overexpress IGF2 were procured from GeneChem (Shanghai, China).

Techniques: Knockdown, Inhibition, Generated, Western Blot, EdU Assay, Plasmid Preparation, Control, Over Expression, Wound Healing Assay, Migration, Cell Culture, Transwell Assay