igf2 protein (Cusabio)
Structured Review

Igf2 Protein, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/igf2 protein/product/Cusabio
Average 93 stars, based on 11 article reviews
Images
1) Product Images from "Malignant Hepatoblast‐Like Cells Sustain Stemness via IGF2‐Dependent Cholesterol Accumulation in Hepatoblastoma"
Article Title: Malignant Hepatoblast‐Like Cells Sustain Stemness via IGF2‐Dependent Cholesterol Accumulation in Hepatoblastoma
Journal: Advanced Science
doi: 10.1002/advs.202407671
Figure Legend Snippet: The insulin signaling pathway and cholesterol metabolism pathway in malignant hepatoblast‐like cells. A,B) Developmental trajectory of hepatocyte cells inferred by monocle2, colored by cell subtypes (A) and CNV levels (B). C) Representative signaling pathways during the developmental trajectory of hepatocyte cells inferred by monocle2. Heatmap showing the dynamic changes in gene expression along the pseudotime trajectory in branch 1 and branch 2. D) Gene set enrichment analysis (GSEA) of malignant HB‐like cells versus all hepatocyte cells in the indicated gene sets. ES, enrichment score; RM, ranked metric; NES, normalized enrichment score; FDR, false discovery rate. E. Heatmap of key gene expression related to the regulation of cholesterol metabolic process (GO: 0090181) and cellular response to insulin stimulus (GO: 0032869) in the three hepatocyte cell types. F) Violin plots showing INS, IGF1, IGF2, INSR, and IGF1R expression levels in the three hepatocyte cell populations. G) Representative IHC images of IGF2 staining of tissue sections. H) The expression levels of key proteins for the insulin signaling and cholesterol metabolic pathways in five pairs of hepatoblastoma and paracancerous tissues. I) Cholesterol concentrations were analyzed in primary hepatoblastoma tumors and paired paracancerous normal liver tissues. J) Lipid droplets (LDs) in primary hepatoblastoma tumors and paired paracancerous liver tissues were stained with BODIPY 493/503. K) BODIPY 493/503 and DUSP9 antibody co‐staining in primary hepatoblastoma tumors.
Techniques Used: Protein-Protein interactions, Gene Expression, Expressing, Staining
Figure Legend Snippet: IGF2 sustains hepatoblastoma stemness via abnormal cholesterol accumulation. A) Effects of IGF2 on the tumorsphere formation of HepG2 cells. Scale bar, 50 µm. Means ± SD are shown ( n = 3). B) The expression level of IGF2‐activated signaling pathway‐related proteins in HepG2 cells treated with IGF2 for five days was analyzed by western blots. C) The expression levels of HB stemness‐related proteins in HepG2 cells treated with IGF2 for five days were analyzed by western blots. D) Pearson's correlation analysis shows the correlation between response to insulin‐like growth factor stimulus (GO: 1990418) and the regulation of cholesterol metabolic process (GO: 0090181) in hepatoblastoma and normal tissue pairs using scRNA sequencing ( n = 14). E) The expression levels of cholesterol metabolic pathway‐related proteins in HepG2 cells treated with IGF2 were analyzed by western blots. F) Cholesterol concentrations were analyzed in HepG2 cells treated with IGF2 for 5 days. G) Lipid droplets (LDs) in HepG2 cells treated with IGF2 for 5 days were stained with BODIPY 493/503. Scale bar, 50 µm. H) Representative images of organoids treated with cholesterol at 0, 10, and 25 µ m on day 5 are shown. Scale bar, 50 µm. I) The expression of HB stemness‐related genes in hepatoblastoma PDOs with or without cholesterol treatment was analyzed by qRT‐PCR. Means ± SD ( n = 3) are shown. J) HepG2‐control cells/HepG2‐IGF2 KD cells were subcutaneously injected into nude mice. Tumor volume changes were examined, and the mice were euthanized 40 days after tumor cell injection. K) The expression levels of IGF2, SREBF2, DUSP9, and LDs in mice tumors were detected by IHC analysis. * p < 0.05, ** p < 0.01, *** p < 0.001 by the Student's t ‐test. L) Cholesterol concentrations were measured in HepG2 cells treated with IGF2 (100 µ m ) and MBCD (1 m m ). M) LDs in HepG2 cells treated with IGF2 (100 µ m ) and MBCD (1 m m ) treatment were stained with BODIPY 493/503. Scale bar, 50 µm. N) Tumorsphere formation assay comparing the effect of IGF2 (100 µ m ) and MBCD (1 m m ) treatments on HepG2 cells. Means ± SD are shown ( n = 3). Scale bar, 50 µm. O) The expression of HB stemness‐related proteins in HepG2 cells treated with IGF2 (100 µ m ) and MBCD (1 m m ) was analyzed by western blots.
Techniques Used: Expressing, Western Blot, Sequencing, Staining, Quantitative RT-PCR, Control, Injection, Paraffin-embedded Immunohistochemistry, Tube Formation Assay
Figure Legend Snippet: SREBF2 mediates abnormal cholesterol accumulation in the activated IGF2 signaling pathway. A) Regulon activity scores of three hepatocyte cell types were calculated using SCENIC. B) GO enrichment analysis for SREBF2 target genes calculated using SCENIC. C) Cholesterol concentrations were analyzed in HepG2 cells with SREBF2 expression. D) LDs were stained with BODIPY 493/503 in HepG2 cells with SREBF2 overexpression. Scale bar, 50 µm. E) Tumorsphere formation assay comparing the effect of SREBF2 on HepG2 cells. Means ± SD are shown ( n = 3). F) The expression of HB stemness‐related proteins was analyzed in HepG2 cells with SREBF2 overexpression using RT‐PCR. G) Schematic diagram of HCD and Fatostain combined treatment. Mice were injected with HepG2 tumor cells subcutaneously after 14 days of HCD feeding. Ten days later, the tumor‐bearing mice were treated with Fatostain at 15 mg kg −1 daily. H) Tumor volume changes were examined, and the mice were euthanized 52 days after treatment. I) Mice were euthanized, and the cholesterol concentrations were measured in tumor tissues. Data represent the mean ± SD of five samples in each group per time point. J) The expression levels of SREBF2, DUSP9, and LDs in mice tumors were analyzed using IHC staining. * p < 0.05, ** p < 0.01, *** p < 0.001 by the Student's t ‐test. K) Cholesterol concentrations were analyzed in HepG2 cells treated with IGF2 and SREBF2 siRNA. L) LDs in HepG2 cells with the indicated treatments were stained with BODIPY 493/503. Scale bar, 50 µm. M) Tumorsphere formation assay comparing the effect of the indicated treatments on HepG2 cells. Means ± SD are shown ( n = 3). N) The expression of HB stemness‐related proteins in HepG2 cells with the indicated treatments was analyzed by western blots.
Techniques Used: Activity Assay, Expressing, Staining, Over Expression, Tube Formation Assay, Reverse Transcription Polymerase Chain Reaction, Injection, Immunohistochemistry, Western Blot
Figure Legend Snippet: Serum IGF2 is a potential diagnostic biomarker for hepatoblastoma patients. A) The column scatter plot shows IGF2 concentrations in serum in the hepatoblastoma group and the control group of children. B) The ROC curve for using serum IGF2 as a diagnostic biomarker. C) The column scatter plot shows serum IGF2 concentration in the PRETEXTI‐II hepatoblastoma group and the PRETEXT III‐IV hepatoblastoma group. D) The column scatter plot shows serum IGF2 concentrations in the before‐treatment hepatoblastoma group and the after‐treatment hepatoblastoma group. E) The column scatter plot shows serum AFP concentrations in the hepatoblastoma group and the control group of children. F) The ROC curve for using serum AFP levels as a diagnostic biomarker. G) The column scatter plot showed serum AFP concentrations in the PRETEXTI‐II hepatoblastoma group and the PRETEXT III‐IV hepatoblastoma group. H) The column scatter plot shows serum AFP concentrations in the before‐treatment hepatoblastoma group and the after‐treatment hepatoblastoma group. p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Diagnostic Assay, Biomarker Discovery, Control, Concentration Assay
Figure Legend Snippet: Schematic diagram of malignant HB‐like cells demonstrating self‐sustaining ability via IGF2‐dependent mechanisms in hepatoblastoma.
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