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Proteintech igf2bp3
Igf2bp3, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/id1/ID1+Antibody/pm41618233-118-18-23
Average 93 stars, based on 42 article reviews

igf2bp3 - by Bioz Stars, 2026-10

93/100 stars

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Ubiquitin Proteomics:

Article Title: Nicotinamide adenine dinucleotide kinase promotes lymph node metastasis of NSCLC via activating ID1 expression through BMP pathway
Article Snippet: The immune signal was detected with a chemiluminescence reagent (Millipore, WBKLS0050), and analyzed with Image Lab software. .. The primary antibodies used were as follows: NADK (Proteintech, 15548-1-AP, 1:2000), beta-Tubulin (Proteintech, 10068-1-AP, 1:3000), GAPDH (Proteintech, 10494-1-AP, 1:10000), Actin (Santa Cruz, sc-8432, 1:3000), Flag-tag (DDDDK-Tag) (Proteintech, 20543-1-AP, 1:3000), Myc-Tag (Cell Signaling Technology, 2276S, 1:3000), HA-tag (Proteintech, 66006-Ig,1:3000), Smad1 (Proteintech, 10429-1-AP, 1:3000), Phospho-Smad1(Ser463/465)/Smad5(Ser463/465)/Smad9(Ser465/467) (Cell Signaling Technology, 13820S, 1:1000), ID1 (Proteintech, 67827Ig, 1:2000), Smurf1 (Proteintech, 55175-1-AP, 1:2000) and ubiquitin (Proteintech, 10201-2-AP, 1:1000). .. The tissue arrays were purchased from Shanghai Outdo Biotech Co., Ltd.

Incubation:

Article Title: ANG secretion predisposes endothelial cells toward angiogenesis in FIN56-induced ferroptotic hepatocellular carcinoma via the BMP6/ID1 signaling pathway.
Article Snippet: Background: Hepatocellular carcinoma (HCC) poses significant challenges due to its high malignancy and limited treatment options.. FIN56 has emerged as a potent inducer of ferroptosis, yet its precise mechanism of action in HCC remains elusive.. Methods: Ferroptosis induction by FIN56 in HCC cells was assessed by quantifying malondialdehyde (MDA), 4hydroxynonenal (4-HNE), reactive oxygen species (ROS), glutathione (GSH) and Liperfluo levels, as well as evaluating changes in mitochondrial morphology.

Recombinant:

Nucleic Acid Electrophoresis:

Article Title: Antiproliferative effect of selexipag active metabolite MRE‐269 on pulmonary arterial smooth muscle cells from patients with chronic thromboembolic pulmonary hypertension
Article Snippet: Normal PASMC‐3 cells were plated on 60‐mm cell culture dishes at 2.5 × 10 5 cells/dish and allowed to adhere overnight in culture medium, then cell growth was arrested by incubation in starvation medium for 48 h. Total cell lysates were prepared with RIPA lysis buffer (Nacalai Tesque) supplemented with 1 mmol/L phenylmethylsulfonyl fluoride (Tocris Biosciences). .. Lysate samples were subjected to sodium dodecyl sulfate‐polyacrylamide gel electrophoresis, transferred to a polyvinylidene difluoride membrane, and probed with antibody specific for ID1 (Proteintech), ID3 (Abcam) or β‐actin (Sigma‐Aldrich). .. Antibodies were detected with the appropriate horseradish peroxidase‐linked secondary antibodies (GE Healthcare) and membranes were developed with the SuperSignal West Femto Maximum Sensitivity Substrate (Thermo Fisher Scientific).

Membrane:

Western Blot:

Article Title: Inhibitor of DNA binding 2 (ID2) regulates the expression of developmental genes and tumorigenesis in ewing sarcoma.
Article Snippet: SDS-PAGE was used to separate proteins, which were then transferred to polyvinylidene difluoride membranes (Sigma). .. Antibodies to the following proteins were used in the immunoblots: ID1 (Biocheck, #195-14, 1:1000), ID2 (Biocheck, #9-2-8, 1:1000), ID2 (Cell Signaling, #D39E8, 1:1000), ID3 (Biocheck, #17-3, 1:2000), puromycin (DSHB, PMY-2A4, 1:500), FLAG (Sigma, F1804, 1:1000), MYC (Proteintech, 60003-2, 1:2000), V5 (Proteintech, 14440-1, 1:2000), and Actin (Cell Signaling, #4970, 1:1000). .. The FLAG-ID1-T2A-MYC-ID2-P2A-V5-ID3 construct was obtained as a gene block (IDT; Coralville, IA) and inserted into the Lenti-X-Tet-One vector (Takara Biology; Mountain View, CA) using NEBuilder HiFi DNA Assembly (NEB; Ipswich, MA).

Image Search Results

Effects of BCL2L1 and ID1 overexpression on hESC differentiation. (B) Quantitative RT-PCR analysis of BCL2L1 and ID1 expression levels in WT, 20q gain, and hESC lines overexpressing BCL2L1, ID1, or both (BCL2L1/ID1). (C) Immunofluorescence staining of the VUB03 cell line: WT, 20q gain, BCL2L1-OE, ID1-OE, and double (BCL2L1 + ID1) overexpression lines. The final condition represents wild-type cells treated with SB and BMP4. Stained markers include PAX6 (yellow; neuroectoderm, panel 1), TFAP2A (magenta; surface ectoderm, panel 2), KRT8 (turquoise; surface ectoderm, panel 2), EPCAM (turquoise; surface ectoderm, panel 3), and OCT4 (magenta; pluripotency, panel 3). (D) Quantification of neuroectoderm immunostaining of BCL2L1-OE, ID1-OE, and double (BCL2L1 + ID1) overexpression lines showing marker intensity similar to . (E) Immunofluorescence staining of VUB03 cells after 14 days of spontaneous differentiation. Stained markers include PAX6 (yellow; neuroectoderm, panel 1), TFAP2A (magenta; surface ectoderm, panel 2), OCT4 (turquoise; pluripotency, panel 2), EPCAM (turquoise; surface ectoderm, panel 3), and KRT8 (magenta; surface ectoderm, panel 3). (F) Quantification of immunostaining of BCL2L1-OE, ID1-OE, and double (BCL2L1 + ID1) overexpression lines after spontaneous differentiation showing marker intensity similar to . (G) Fraction of marker-positive cells after 8 days of neuroectoderm differentiation. (H) Fraction of marker-positive cells after 14 days of spontaneous differentiation.

Journal: bioRxiv

Article Title: Increases in BCL2L1 and ID1 dosage synergistically drive fate bias and competitive advantage in human pluripotent stem cells

doi: 10.64898/2026.03.26.714405

Figure Lengend Snippet: Effects of BCL2L1 and ID1 overexpression on hESC differentiation. (B) Quantitative RT-PCR analysis of BCL2L1 and ID1 expression levels in WT, 20q gain, and hESC lines overexpressing BCL2L1, ID1, or both (BCL2L1/ID1). (C) Immunofluorescence staining of the VUB03 cell line: WT, 20q gain, BCL2L1-OE, ID1-OE, and double (BCL2L1 + ID1) overexpression lines. The final condition represents wild-type cells treated with SB and BMP4. Stained markers include PAX6 (yellow; neuroectoderm, panel 1), TFAP2A (magenta; surface ectoderm, panel 2), KRT8 (turquoise; surface ectoderm, panel 2), EPCAM (turquoise; surface ectoderm, panel 3), and OCT4 (magenta; pluripotency, panel 3). (D) Quantification of neuroectoderm immunostaining of BCL2L1-OE, ID1-OE, and double (BCL2L1 + ID1) overexpression lines showing marker intensity similar to . (E) Immunofluorescence staining of VUB03 cells after 14 days of spontaneous differentiation. Stained markers include PAX6 (yellow; neuroectoderm, panel 1), TFAP2A (magenta; surface ectoderm, panel 2), OCT4 (turquoise; pluripotency, panel 2), EPCAM (turquoise; surface ectoderm, panel 3), and KRT8 (magenta; surface ectoderm, panel 3). (F) Quantification of immunostaining of BCL2L1-OE, ID1-OE, and double (BCL2L1 + ID1) overexpression lines after spontaneous differentiation showing marker intensity similar to . (G) Fraction of marker-positive cells after 8 days of neuroectoderm differentiation. (H) Fraction of marker-positive cells after 14 days of spontaneous differentiation.

Article Snippet: The ID1 expression plasmid (TFORF2860) was obtained from Addgene (plasmid #143643), with ID1 expression driven by the EF-1α promoter.

Techniques: Over Expression, Quantitative RT-PCR, Expressing, Immunofluorescence, Staining, Immunostaining, Marker

EmC leads to induction of genes related to lung metastasis. A, qRT-PCR of mRNA levels for indicated genes in SUM149 and MDA-MB-468 cells under the indicated culture conditions ( n = 3). B, Differential expression of the indicated genes derived from the scRNA-seq data comparing EmC vs. SphC in SUM149 and IBC-3 cells as indicated. C, qRT-PCR (top, n = 3) of ID1 expression in SUM149 and MDA-MB-468 cultures as indicated. D, Western blot analysis of ID1 expression of cells as in C . Actin served as a loading control. E, Western blot analysis of ID1 and ID3 proteins in established SUM149 EmC cells that were treated with AGX51 at the indicated concentrations for 3 days. Actin served as a loading control. F, FC in viable SUM149 and MDA-MB-468 cells in established EmC following AGX51 treatment at the indicated concentrations for 3 days ( n = 3). G, FC in viable SUM149 and MDA-MB-468 cells in established EmC and SphC following AGX51 treatment (100 μmol/L) for 3 days ( n = 3). Quantitative data are shown as mean ± SEM, *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; n.s., not significant.

Journal: Cancer Research Communications

Article Title: 3D “Emboli” Culture Models Epithelial Breast Cancer Cell Oxidative Mitochondrial Metabolism with Relevance for Lung Metastasis

doi: 10.1158/2767-9764.CRC-25-0587

Figure Lengend Snippet: EmC leads to induction of genes related to lung metastasis. A, qRT-PCR of mRNA levels for indicated genes in SUM149 and MDA-MB-468 cells under the indicated culture conditions ( n = 3). B, Differential expression of the indicated genes derived from the scRNA-seq data comparing EmC vs. SphC in SUM149 and IBC-3 cells as indicated. C, qRT-PCR (top, n = 3) of ID1 expression in SUM149 and MDA-MB-468 cultures as indicated. D, Western blot analysis of ID1 expression of cells as in C . Actin served as a loading control. E, Western blot analysis of ID1 and ID3 proteins in established SUM149 EmC cells that were treated with AGX51 at the indicated concentrations for 3 days. Actin served as a loading control. F, FC in viable SUM149 and MDA-MB-468 cells in established EmC following AGX51 treatment at the indicated concentrations for 3 days ( n = 3). G, FC in viable SUM149 and MDA-MB-468 cells in established EmC and SphC following AGX51 treatment (100 μmol/L) for 3 days ( n = 3). Quantitative data are shown as mean ± SEM, *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; n.s., not significant.

Article Snippet: Immunohistochemistry was performed according to standard procedures with primary antibodies for ID1 at 1:50 (Cell Signaling Technology #23369), Ki67 at 1:200 (Cell Signaling Technology #9027), or isotype control rabbit monoclonal IgG (Cell Signaling Technology # 3900).

Techniques: Quantitative RT-PCR, Quantitative Proteomics, Derivative Assay, Expressing, Western Blot, Control

Assessment of the cell line identity and the genomic integrity of the six MSA patient-derived iPSCs. (A) Short tandem repeat profiling provided the number of repeating units of 16 polymorphic microsatellite loci, to compare the donor fibroblast cells (reference) and the generated iPSCs and verify their origin. (B) G-banding revealed that the six iPSC lines showed a normal diploid karyotype (n = 46) and matched the sex of the donor patient. (C) Digital PCR allowed us to screen whether specific genomic regions accumulated duplications that may give a strong selective survival or growth advantage to iPSCs. Example of the scatter digital PCR plots displaying simultaneously (1) FAM signals, shown in purple and green to detect the target gene ( ID1 , NCAPD2 , PITX1 , RPS6KB1 , SOAT1 , or STS ), which are located in the 6 most recurrent abnormal regions; and (2) VIM signals, shown in orange and green to detect the reference gene, RPP30 . The ratio between the number of copies of the target gene and of the reference gene was used to determine the normal 2-copy number or copy number variations. The plots were obtained through QuantStudio 3D Digital PCR system. In all cases, we obtained 2-copy number (D) Quantitative Real Time RT-PCR was used for confirming the absence of the Sendai virus in the iPSC lines after 8 passages, through four primer sets (SeV, KOS, Klf4 and c-Myc). Box and Whisker plots depict in log10 scale the gene expression relative to GAPDH gene and normalized to the 7 days post-transduction fibroblasts, calculated by the 2(-ΔΔC(T)) method. In all iPSC clones, the expression levels of the SeV RNA were very low, reaching the limit of detection. Data are shown as the mean ± s.d. n = 3.

Journal: Frontiers in Immunology

Article Title: Generation and characterization of human induced pluripotent stem cells from neuropathologically confirmed multiple system atrophy patient-derived fibroblasts

doi: 10.3389/fimmu.2026.1641981

Figure Lengend Snippet: Assessment of the cell line identity and the genomic integrity of the six MSA patient-derived iPSCs. (A) Short tandem repeat profiling provided the number of repeating units of 16 polymorphic microsatellite loci, to compare the donor fibroblast cells (reference) and the generated iPSCs and verify their origin. (B) G-banding revealed that the six iPSC lines showed a normal diploid karyotype (n = 46) and matched the sex of the donor patient. (C) Digital PCR allowed us to screen whether specific genomic regions accumulated duplications that may give a strong selective survival or growth advantage to iPSCs. Example of the scatter digital PCR plots displaying simultaneously (1) FAM signals, shown in purple and green to detect the target gene ( ID1 , NCAPD2 , PITX1 , RPS6KB1 , SOAT1 , or STS ), which are located in the 6 most recurrent abnormal regions; and (2) VIM signals, shown in orange and green to detect the reference gene, RPP30 . The ratio between the number of copies of the target gene and of the reference gene was used to determine the normal 2-copy number or copy number variations. The plots were obtained through QuantStudio 3D Digital PCR system. In all cases, we obtained 2-copy number (D) Quantitative Real Time RT-PCR was used for confirming the absence of the Sendai virus in the iPSC lines after 8 passages, through four primer sets (SeV, KOS, Klf4 and c-Myc). Box and Whisker plots depict in log10 scale the gene expression relative to GAPDH gene and normalized to the 7 days post-transduction fibroblasts, calculated by the 2(-ΔΔC(T)) method. In all iPSC clones, the expression levels of the SeV RNA were very low, reaching the limit of detection. Data are shown as the mean ± s.d. n = 3.

Article Snippet: ID1 , Hs01892845_cn , FAM , 20q11 , hg38|31605682-31605761 , 79 bp , MseI, HindIII, CviQI.

Techniques: Derivative Assay, Generated, Digital PCR, Quantitative RT-PCR, Virus, Whisker Assay, Gene Expression, Transduction, Clone Assay, Expressing

Journal: BMC Musculoskeletal Disorders

Article Title: The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability

doi: 10.1186/s12891-026-09527-0

Figure Lengend Snippet: ID1 modulates malignant behaviors in OS cells. A : ID1 expression profile in the GSE253548 dataset. B : RT-qPCR analysis of ID1 mRNA levels across cell groups. C : Western blot detection of ID1 protein expression. D : Validation of ID1 knockdown efficiency by RT-qPCR. E : CCK-8 assay assessing cellular proliferation. F : Colony formation capacity quantified across experimental groups. G : Scratch assay evaluating cell migration ability, scale bar = 400 μm. H : Transwell invasion assay with representative images, scale bar = 200 μm. Data are presented as mean ± SEM. *** P < 0.001, **** P < 0.0001. Statistical analyses were performed using independent-samples t-test or one-way ANOVA followed by Tukey’s post hoc test. All experiments were performed in triplicate.

Article Snippet: To determine ID1 mRNA stability, infected MG-63 cells were exposed to 4 μg/mL actinomycin D (HY-17559, MedChemExpress), a transcriptional elongation inhibitor, for defined durations (0/2/4/6 hours).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Biomarker Discovery, Knockdown, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay

Journal: BMC Musculoskeletal Disorders

Article Title: The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability

doi: 10.1186/s12891-026-09527-0

Figure Lengend Snippet: Identification of OS-specific RNA-binding proteins regulating ID1 and mechanistic predictions. A : Volcano plot of DEGs in the GSE253548 dataset. B : Venn diagram intersecting ENCORI-predicted RBPs with DEGs. C : Feature selection by LASSO regression. D : SVM-RFE algorithm-derived feature genes. E : Variable importance ranking from random forest analysis. F : Venn diagram overlapping feature genes identified by LASSO, SVM-RFE, and random forest. G : IGF2BP3 expression profile in the GSE253548 dataset. H : RT-qPCR analysis of IGF2BP3 mRNA levels. I : Western blot detection of IGF2BP3 protein expression. J : SRAMP-predicted m 6 A modification site on ID1 mRNA. K : Secondary structure of the m 6 A-modified site at 782 nt on ID1 mRNA. L : MeRIP-qPCR quantification of ID1 m 6 A modification levels. M : RM2Target-predicted m 6 A-mediated interaction between IGF2BP3 and ID1. N : Spearman correlation of IGF2BP3 and ID1 expression. Data are presented as mean ± SEM. ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical analyses were performed using independent-samples t -test or one-way ANOVA followed by Tukey’s post hoc test. All experiments were performed in triplicate.

Techniques: RNA Binding Assay, Selection, Derivative Assay, Expressing, Quantitative RT-PCR, Western Blot, Modification

IGF2BP3 regulates ID1 to modulate malignant behaviors in OS Cells. A - B : RT-qPCR analysis of IGF2BP3 expression in engineered cells. C : RT-qPCR detection of ID1 mRNA levels. D : Western blot analysis of ID1 protein expression. E : RIP-qPCR demonstrating IGF2BP3-ID1 mRNA interaction, with RIP efficiency validated by Western blot. F : Schematic of ID1-WT/MUT CDS and their dual-luciferase reporter constructs. G : Dual-luciferase reporter gene assay results. H : RT-qPCR for ID1 mRNA expression in cells at different time points (0, 2, 4, 6 h) after actinomycin D treatment. I : Western blot for IGF2BP3 and ID1 expression in cells. J : CCK-8 assay assessing cellular proliferation. K : Colony formation capacity quantified across experimental groups. L : Scratch assay evaluating cell migration ability, scale bar = 400 μm. M : Transwell invasion assay with representative images, scale bar = 200 μm. Data are presented as mean ± SEM. ns P > 0.05, **** P < 0.0001. Statistical analyses were performed using independent-samples t-test or one-way ANOVA followed by Tukey’s post hoc test. All experiments were performed in triplicate.

Journal: BMC Musculoskeletal Disorders

Article Title: The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability

doi: 10.1186/s12891-026-09527-0

Figure Lengend Snippet: IGF2BP3 regulates ID1 to modulate malignant behaviors in OS Cells. A - B : RT-qPCR analysis of IGF2BP3 expression in engineered cells. C : RT-qPCR detection of ID1 mRNA levels. D : Western blot analysis of ID1 protein expression. E : RIP-qPCR demonstrating IGF2BP3-ID1 mRNA interaction, with RIP efficiency validated by Western blot. F : Schematic of ID1-WT/MUT CDS and their dual-luciferase reporter constructs. G : Dual-luciferase reporter gene assay results. H : RT-qPCR for ID1 mRNA expression in cells at different time points (0, 2, 4, 6 h) after actinomycin D treatment. I : Western blot for IGF2BP3 and ID1 expression in cells. J : CCK-8 assay assessing cellular proliferation. K : Colony formation capacity quantified across experimental groups. L : Scratch assay evaluating cell migration ability, scale bar = 400 μm. M : Transwell invasion assay with representative images, scale bar = 200 μm. Data are presented as mean ± SEM. ns P > 0.05, **** P < 0.0001. Statistical analyses were performed using independent-samples t-test or one-way ANOVA followed by Tukey’s post hoc test. All experiments were performed in triplicate.

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Luciferase, Construct, Reporter Gene Assay, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay

The METTL3-IGF2BP3 axis mediates m 6 A-dependent regulation of ID1 expression and stability. A : METTL3 expression in GSE253548 dataset. B - C : METTL3 expression in cell lines via RT-qPCR (B) and Western blot (C). D : RM2Target prediction of METTL3-ID1 interaction. E : Spearman correlation between METTL3 and ID1 expression. F - G : METTL3 expression validation in engineered cells. H : MeRIP-qPCR analysis of ID1 m6A modification levels. I : RIP-qPCR analysis of the interaction between METTL3 and ID1 mRNA, with the efficiency of the RIP assay validated by Western blot. J : RIP-qPCR detection of IGF2BP3-ID1 mRNA interaction. K : MeRIP-qPCR analysis of ID1 m6A modification levels in MG-63 cells with endogenous METTL3 knockdown. L : RIP-qPCR analysis of the interaction between IGF2BP3 and ID1 mRNA in MG-63 cells with endogenous METTL3 knockdown. M - N : ID1 mRNA (M) and protein (N) expression under indicated treatments. O : RNA stability assay under actinomycin D treatment (0, 2, 4, 6 h). Data are presented as mean ± SEM. ns P > 0.05, *** P < 0.001, **** P < 0.0001. Statistical analyses were performed using independent-samples t-test or one-way ANOVA followed by Tukey’s post hoc test. All experiments were performed in triplicate.

Journal: BMC Musculoskeletal Disorders

Article Title: The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability

doi: 10.1186/s12891-026-09527-0

Figure Lengend Snippet: The METTL3-IGF2BP3 axis mediates m 6 A-dependent regulation of ID1 expression and stability. A : METTL3 expression in GSE253548 dataset. B - C : METTL3 expression in cell lines via RT-qPCR (B) and Western blot (C). D : RM2Target prediction of METTL3-ID1 interaction. E : Spearman correlation between METTL3 and ID1 expression. F - G : METTL3 expression validation in engineered cells. H : MeRIP-qPCR analysis of ID1 m6A modification levels. I : RIP-qPCR analysis of the interaction between METTL3 and ID1 mRNA, with the efficiency of the RIP assay validated by Western blot. J : RIP-qPCR detection of IGF2BP3-ID1 mRNA interaction. K : MeRIP-qPCR analysis of ID1 m6A modification levels in MG-63 cells with endogenous METTL3 knockdown. L : RIP-qPCR analysis of the interaction between IGF2BP3 and ID1 mRNA in MG-63 cells with endogenous METTL3 knockdown. M - N : ID1 mRNA (M) and protein (N) expression under indicated treatments. O : RNA stability assay under actinomycin D treatment (0, 2, 4, 6 h). Data are presented as mean ± SEM. ns P > 0.05, *** P < 0.001, **** P < 0.0001. Statistical analyses were performed using independent-samples t-test or one-way ANOVA followed by Tukey’s post hoc test. All experiments were performed in triplicate.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Biomarker Discovery, Modification, Knockdown, Stability Assay

The METTL3-IGF2BP3 axis mediates ID1-dependent malignant behaviors in OS cells. A : CCK-8 assay assessing cell proliferation. B : Colony formation assay quantifying clonogenic capacity. C : Scratch wound healing assay evaluating migration, scale bar = 400 μm. D : Transwell invasion assay, scale bar = 200 μm. E : Cell proliferation evaluated by CCK8 assay. F : Colony formation assay to assess colony numbers. G : Scratch assay to evaluate the migration ability of cells, scale bar = 400 μm. H : Transwell assay to assess the invasion ability of cells, scale bar = 200 μm. Data are presented as mean ± SEM. ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical analyses were performed using independent-samples t-test or one-way ANOVA followed by Tukey’s post hoc test. All experiments were performed in triplicate.

Journal: BMC Musculoskeletal Disorders

Article Title: The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability

doi: 10.1186/s12891-026-09527-0

Figure Lengend Snippet: The METTL3-IGF2BP3 axis mediates ID1-dependent malignant behaviors in OS cells. A : CCK-8 assay assessing cell proliferation. B : Colony formation assay quantifying clonogenic capacity. C : Scratch wound healing assay evaluating migration, scale bar = 400 μm. D : Transwell invasion assay, scale bar = 200 μm. E : Cell proliferation evaluated by CCK8 assay. F : Colony formation assay to assess colony numbers. G : Scratch assay to evaluate the migration ability of cells, scale bar = 400 μm. H : Transwell assay to assess the invasion ability of cells, scale bar = 200 μm. Data are presented as mean ± SEM. ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical analyses were performed using independent-samples t-test or one-way ANOVA followed by Tukey’s post hoc test. All experiments were performed in triplicate.

Techniques: CCK-8 Assay, Colony Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Transwell Assay

Effects of METTL3 and IGF2BP3 inhibitors on ID1-mediated malignant behaviors of OS cells. A : RT-qPCR analysis of ID1 expression in each group of cells. B : WB analysis of ID1 expression in each group of cells. C : RT-qPCR analysis of ID1 mRNA levels at different time points (0, 2, 4, 6 h) following actinomycin D treatment. D : CCK-8 assay assessing cell proliferation. E : Colony formation assay evaluating colony numbers in each group. F : Wound healing assay assessing cell migration ability; scale bar = 400 μm. G : Transwell assay assessing cell invasion ability; scale bar = 200 μm. Data are presented as mean ± SEM. **** P < 0.0001. Statistical analyses were performed using one-way ANOVA followed by Tukey’s post hoc test. All cell experiments were repeated three times.

Journal: BMC Musculoskeletal Disorders

Article Title: The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability

doi: 10.1186/s12891-026-09527-0

Figure Lengend Snippet: Effects of METTL3 and IGF2BP3 inhibitors on ID1-mediated malignant behaviors of OS cells. A : RT-qPCR analysis of ID1 expression in each group of cells. B : WB analysis of ID1 expression in each group of cells. C : RT-qPCR analysis of ID1 mRNA levels at different time points (0, 2, 4, 6 h) following actinomycin D treatment. D : CCK-8 assay assessing cell proliferation. E : Colony formation assay evaluating colony numbers in each group. F : Wound healing assay assessing cell migration ability; scale bar = 400 μm. G : Transwell assay assessing cell invasion ability; scale bar = 200 μm. Data are presented as mean ± SEM. **** P < 0.0001. Statistical analyses were performed using one-way ANOVA followed by Tukey’s post hoc test. All cell experiments were repeated three times.

Techniques: Quantitative RT-PCR, Expressing, CCK-8 Assay, Colony Assay, Wound Healing Assay, Migration, Transwell Assay

The METTL3-IGF2BP3 axis mediates ID1-dependent tumor growth in vivo. A : Western blot analysis of METTL3 and ID1 expression in tumor tissues from each group of mice. B : Western blot analysis of IGF2BP3 and ID1 expression in tumor tissues from each group of mice. C - D : Changes in tumor volume in each group of mice. E - F : Representative images of tumors from each group of mice. G - H : Tumor weights in each group of mice. I - J : Representative immunohistochemical images of Ki67 staining and quantification of Ki67-positive area percentage in tumor tissues from each group of mice, scale bar = 100 μm. N = 6. Data are presented as mean ± SEM. ns P > 0.05, *** P < 0.001, **** P < 0.0001. Statistical analyses were performed using one-way ANOVA followed by Tukey’s post hoc test.

Journal: BMC Musculoskeletal Disorders

Article Title: The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability

doi: 10.1186/s12891-026-09527-0

Figure Lengend Snippet: The METTL3-IGF2BP3 axis mediates ID1-dependent tumor growth in vivo. A : Western blot analysis of METTL3 and ID1 expression in tumor tissues from each group of mice. B : Western blot analysis of IGF2BP3 and ID1 expression in tumor tissues from each group of mice. C - D : Changes in tumor volume in each group of mice. E - F : Representative images of tumors from each group of mice. G - H : Tumor weights in each group of mice. I - J : Representative immunohistochemical images of Ki67 staining and quantification of Ki67-positive area percentage in tumor tissues from each group of mice, scale bar = 100 μm. N = 6. Data are presented as mean ± SEM. ns P > 0.05, *** P < 0.001, **** P < 0.0001. Statistical analyses were performed using one-way ANOVA followed by Tukey’s post hoc test.

Techniques: In Vivo, Western Blot, Expressing, Immunohistochemical staining, Staining

Mechanistic diagram of METTL3-IGF2BP3-mediated ID1 in promoting osteosarcoma progression

Journal: BMC Musculoskeletal Disorders

Article Title: The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability

doi: 10.1186/s12891-026-09527-0

Figure Lengend Snippet: Mechanistic diagram of METTL3-IGF2BP3-mediated ID1 in promoting osteosarcoma progression

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