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nsd2 targeting (Vector Laboratories)

Name: nsd2 targeting
Brand: Vector Laboratories
Rating: 96 (7594 reviews)

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Vector Laboratories nsd2 targeting
Nsd2 Targeting, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 96/100, based on 7594 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 7594 article reviews

nsd2 targeting - by Bioz Stars, 2026-02

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NUP62 affects NSD2 transcription by facilitating the nuclear transport of the transcription factor E2F1. a Gene set enrichment analysis (GSEA) identified distinct induction of the target gene signatures of the transcription factor E2F1 in human dental pulp stem cells (HDPSCs) with and without NUP62 overexpression. b Western blot analysis of E2F1 levels in the nucleoplasm and cytoplasm of HDPSCs transfected with the lentiviral vector or overexpressing NUP62. c Quantitative analysis of the E2F1 Western blotting results ( n = 3). d Mapping of E2F1 ChIP-seq reads to the NSD2 genomic locus. The figure was obtained from the Cristrome database. e, f Western blot analyses of E2F1 and NSD2 in HDPSCs transfected with control or E2F1 siRNA. g , h mRNA levels of E2F1 and NSD2 in HDPSCs transfected with control or E2F1 siRNA ( n = 3). i ChIP‒qPCR revealed that E2F1 binds to the promoter region of NSD2 ( n = 3). j Luminescence analysis of 293 T cells following co-transfection with an empty vector or overexpressing E2F1, a promoter luciferase reporter (wild type), and a Renilla control ( n = 3). k Representative images of immunofluorescence staining of E2F1. Scale bar, 50 μm. l Nuclear/Cytoplasmic fluorescence ratio of E2F1 ( n = 10). * P < 0.05, ** P < 0.01 and *** P < 0.001

Journal: International Journal of Oral Science

Article Title: NUP62 alleviates senescence and promotes the stemness of human dental pulp stem cells via NSD2-dependent epigenetic reprogramming

doi: 10.1038/s41368-025-00362-y

Figure Lengend Snippet: NUP62 affects NSD2 transcription by facilitating the nuclear transport of the transcription factor E2F1. a Gene set enrichment analysis (GSEA) identified distinct induction of the target gene signatures of the transcription factor E2F1 in human dental pulp stem cells (HDPSCs) with and without NUP62 overexpression. b Western blot analysis of E2F1 levels in the nucleoplasm and cytoplasm of HDPSCs transfected with the lentiviral vector or overexpressing NUP62. c Quantitative analysis of the E2F1 Western blotting results ( n = 3). d Mapping of E2F1 ChIP-seq reads to the NSD2 genomic locus. The figure was obtained from the Cristrome database. e, f Western blot analyses of E2F1 and NSD2 in HDPSCs transfected with control or E2F1 siRNA. g , h mRNA levels of E2F1 and NSD2 in HDPSCs transfected with control or E2F1 siRNA ( n = 3). i ChIP‒qPCR revealed that E2F1 binds to the promoter region of NSD2 ( n = 3). j Luminescence analysis of 293 T cells following co-transfection with an empty vector or overexpressing E2F1, a promoter luciferase reporter (wild type), and a Renilla control ( n = 3). k Representative images of immunofluorescence staining of E2F1. Scale bar, 50 μm. l Nuclear/Cytoplasmic fluorescence ratio of E2F1 ( n = 10). * P < 0.05, ** P < 0.01 and *** P < 0.001

Article Snippet: Small interfering RNAs (siRNAs) targeting NSD2 or E2F1 were purchased from RiboBio Co., Ltd (Guangzhou, China) and transfected into HDPSCs at a concentration of 25 nmol/L with JetPrimer (No. 101000046, France).

Techniques: Over Expression, Western Blot, Transfection, Plasmid Preparation, ChIP-sequencing, Control, Cotransfection, Luciferase, Immunofluorescence, Staining, Fluorescence

NSRP1 regulated the AS of many oncogenes . A , Volcano plots of significant altered AS events in MCF7 cells with transfection of siNSRP1s or siControl. B , Pie plot of the proportion of 5 AS types of significant altered AS events (siNSRP1s vs. siControl). C , distribution of AS events in locations of transcripts. D , KEGG enrichment of genes with altered AS events. The genes regulating the IFN pathway were labeled with bold style. E–G , Sashimi plots of altered AS events in NSD2, IL4R, and HRAS. RT-PCR was also performed to detect the inclusion of exons in NSD2, IL4R, and HRAS. Comparison by one-way ANOVA followed by the Tukey test ( E–G : n = 3 replicates/group). Error bars represent SD.

Journal: The Journal of Biological Chemistry

Article Title: Downregulation of the splicing regulator NSRP1 confers resistance to CDK4/6 inhibitors via activation of interferon signaling in breast cancer

doi: 10.1016/j.jbc.2024.108070

Figure Lengend Snippet: NSRP1 regulated the AS of many oncogenes . A , Volcano plots of significant altered AS events in MCF7 cells with transfection of siNSRP1s or siControl. B , Pie plot of the proportion of 5 AS types of significant altered AS events (siNSRP1s vs. siControl). C , distribution of AS events in locations of transcripts. D , KEGG enrichment of genes with altered AS events. The genes regulating the IFN pathway were labeled with bold style. E–G , Sashimi plots of altered AS events in NSD2, IL4R, and HRAS. RT-PCR was also performed to detect the inclusion of exons in NSD2, IL4R, and HRAS. Comparison by one-way ANOVA followed by the Tukey test ( E–G : n = 3 replicates/group). Error bars represent SD.

Article Snippet: Control siRNA and siRNAs targeting NSRP1 or NSD2 were synthesized by GenePharma.

Techniques: Transfection, Labeling, Reverse Transcription Polymerase Chain Reaction, Comparison

The inclusion of NSD2 exon 2 was elevated in breast cancer . A , RT-PCR detection of the inclusion of NSD2 exon 2 in MCF7 and MCF7-PalR cells. B , the PSI values of NSD2 exon 2 between breast tumors and normal tissues were compared. C , the association between the PSI values of NSD2 exon 2 and the overall survival of patients with breast cancer was analyzed with the Kaplan-Meier method. D , RT-PCR detection of the inclusion of NSD2 exon 2 in 15 pairs of breast tumors and matched normal tissues from patients diagnosed with ER+/Her2-breast cancer. Comparison by Student’s t test ( A : n = 3 replicates/group, unpaired; B : n = 3 for Normal, n = 143 for Tumor, unpaired; D, n = 14 samples/group, paired) or Kaplan-Meier analysis ( C ). Error bars represent SD.

Journal: The Journal of Biological Chemistry

Article Title: Downregulation of the splicing regulator NSRP1 confers resistance to CDK4/6 inhibitors via activation of interferon signaling in breast cancer

doi: 10.1016/j.jbc.2024.108070

Figure Lengend Snippet: The inclusion of NSD2 exon 2 was elevated in breast cancer . A , RT-PCR detection of the inclusion of NSD2 exon 2 in MCF7 and MCF7-PalR cells. B , the PSI values of NSD2 exon 2 between breast tumors and normal tissues were compared. C , the association between the PSI values of NSD2 exon 2 and the overall survival of patients with breast cancer was analyzed with the Kaplan-Meier method. D , RT-PCR detection of the inclusion of NSD2 exon 2 in 15 pairs of breast tumors and matched normal tissues from patients diagnosed with ER+/Her2-breast cancer. Comparison by Student’s t test ( A : n = 3 replicates/group, unpaired; B : n = 3 for Normal, n = 143 for Tumor, unpaired; D, n = 14 samples/group, paired) or Kaplan-Meier analysis ( C ). Error bars represent SD.

Article Snippet: Control siRNA and siRNAs targeting NSRP1 or NSD2 were synthesized by GenePharma.

Techniques: Reverse Transcription Polymerase Chain Reaction, Comparison

$NSRP1 negatively regulated NSD2 protein expression . A , analysis of the structures of NSD2 transcripts with or without exon 2. B , ribo-Seq data showed that peaks were observed in the exon 2 region in the NSD2 transcript. C , the polysome profiling curves of siControl, siNSRP1-1, and siNSRP1-2 MCF7 cells were indicated. D , RT-qPCR was performed to detect the ratio of NSD2 mRNA in polysomal (Poly) and subpolysomal (Subpoly) fractions from polysome profiling of siControl, siNSRP1-1, and siNSRP1-2 MCF7 cells. E and F , Western blotting detection of protein levels of NSD2 in MCF7 ( E ) and MCF7-PalR ( F ) cells with transfection of siNSRP1s or siControl. G , Western blotting detection of protein levels of NSD2 in MCF7-PalR cells with transfection of pcDNA3 or pcDNA3-NSRP1. H and I , Western blotting detection of protein levels of NSD2 and IFN-stimulated genes in MCF7 or MCF7-PalR cells with transfection of siNSD2s or siControl. J , Western blotting detection of protein levels of NSD2 and IFN-stimulated genes in MCF7 cells with overexpression of NSD2. K , Western blotting detection of protein levels of NSRP1, NSD2, and IFN-stimulated genes in MCF7-PalR cells with overexpression of NSRP1 or NSD2 or NSRP1 + NSD2. Comparison by one-way ANOVA followed by the Tukey test ( D–F , H , I , K , and L : n = 3 replicates/group) or Student’s t test ( G and J : n = 3 replicates/group, unpaired). Error bars represent SD.$

Journal: The Journal of Biological Chemistry

Article Title: Downregulation of the splicing regulator NSRP1 confers resistance to CDK4/6 inhibitors via activation of interferon signaling in breast cancer

doi: 10.1016/j.jbc.2024.108070

Figure Lengend Snippet: NSRP1 negatively regulated NSD2 protein expression . A , analysis of the structures of NSD2 transcripts with or without exon 2. B , ribo-Seq data showed that peaks were observed in the exon 2 region in the NSD2 transcript. C , the polysome profiling curves of siControl, siNSRP1-1, and siNSRP1-2 MCF7 cells were indicated. D , RT-qPCR was performed to detect the ratio of NSD2 mRNA in polysomal (Poly) and subpolysomal (Subpoly) fractions from polysome profiling of siControl, siNSRP1-1, and siNSRP1-2 MCF7 cells. E and F , Western blotting detection of protein levels of NSD2 in MCF7 ( E ) and MCF7-PalR ( F ) cells with transfection of siNSRP1s or siControl. G , Western blotting detection of protein levels of NSD2 in MCF7-PalR cells with transfection of pcDNA3 or pcDNA3-NSRP1. H and I , Western blotting detection of protein levels of NSD2 and IFN-stimulated genes in MCF7 or MCF7-PalR cells with transfection of siNSD2s or siControl. J , Western blotting detection of protein levels of NSD2 and IFN-stimulated genes in MCF7 cells with overexpression of NSD2. K , Western blotting detection of protein levels of NSRP1, NSD2, and IFN-stimulated genes in MCF7-PalR cells with overexpression of NSRP1 or NSD2 or NSRP1 + NSD2. Comparison by one-way ANOVA followed by the Tukey test ( D–F , H , I , K , and L : n = 3 replicates/group) or Student’s t test ( G and J : n = 3 replicates/group, unpaired). Error bars represent SD.

Article Snippet: Control siRNA and siRNAs targeting NSRP1 or NSD2 were synthesized by GenePharma.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Transfection, Over Expression, Comparison

Chemical structures of representative NSD2 inhibitors and degraders 10–16.

Journal: Journal of medicinal chemistry

Article Title: Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2)

doi: 10.1021/acs.jmedchem.3c00948

Figure Lengend Snippet: Chemical structures of representative NSD2 inhibitors and degraders 10–16.

Article Snippet: Both NSD2 and its target gene HDAC2 were revealed to activate the NF-κB signaling pathway inducing the occurrence and progression of inflammation by promoting the release of proinflammatory cytokines.204 Meanwhile, NSD2 can modulate the envelope protein (protein E) of SARS-CoV2 via interactions with BRD4, suggesting that NSD2 may play an important role in the progression of SARS-CoV2.204 Proteolysis protein chimeras (PROTACs) targeting NSD2 degradation are being developed as valuable tools to explore the role of NSD2 in SARS-CoV2 and/or as potential therapeutic agents to treat COVID-19, a SARS-CoV2-related coronavirus disease (https://www.mitacs.ca/en/projects/development-targeted-degradation-nuclear-receptor-binding-set-domain-protein-2-nsd2).

Techniques:

The biological functions of NSD2 and underlying mechanisms.

Journal: Journal of medicinal chemistry

Article Title: Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2)

doi: 10.1021/acs.jmedchem.3c00948

Figure Lengend Snippet: The biological functions of NSD2 and underlying mechanisms.

Techniques:

Overview of various cancers associated with NSD lysine methyltransferases (KMTases) dysregulation.

Journal: Journal of medicinal chemistry

Article Title: Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2)

doi: 10.1021/acs.jmedchem.3c00948

Figure Lengend Snippet: Overview of various cancers associated with NSD lysine methyltransferases (KMTases) dysregulation.

Techniques: Migration, Mutagenesis, Activity Assay, Transformation Assay, Expressing, DNA Synthesis

Crystal structure of compound 50 (MR837) in complex with NSD2-PWWP1 domain (PDB ID: 6UE6). Hydrogen bonds formed between 50 and the key residues in the NSD2-PWWP1 domain are highlighted by red dashed lines. Compound 50 is shown as yellow sticks. Key residues ALA-270, TYR-233, TRP-236, PHE-266, and VAL-230 in the NSD2-PWWP1 domain are shown as green sticks.

Journal: Journal of medicinal chemistry

Article Title: Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2)

doi: 10.1021/acs.jmedchem.3c00948

Figure Lengend Snippet: Crystal structure of compound 50 (MR837) in complex with NSD2-PWWP1 domain (PDB ID: 6UE6). Hydrogen bonds formed between 50 and the key residues in the NSD2-PWWP1 domain are highlighted by red dashed lines. Compound 50 is shown as yellow sticks. Key residues ALA-270, TYR-233, TRP-236, PHE-266, and VAL-230 in the NSD2-PWWP1 domain are shown as green sticks.

Techniques:

(a) SAM crystal structure in complex with NSD2-SET domain (PDB ID: 5LSU). SAM is shown as cyan sticks; (b) Crystal structure of DNA in complex with NSD2-PWWP1 domain (PDB ID: 5VC8). The key residues LYS-304, LYS-309, and LYS-312 in NSD2-PWWP1 domain that form direct electrostatic interactions with the DNA phosphate backbone are shown as cyan sticks; and (c) The structures of three NSD2 isoforms (NSD2-long, NSD2-short, and RE-IIBP) that are composed of multiple domains, including PWWP domain, PHD domain, SET domain (AWS/pre-SET, SET, and post-SET), etc.

Journal: Journal of medicinal chemistry

Article Title: Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2)

doi: 10.1021/acs.jmedchem.3c00948

Figure Lengend Snippet: (a) SAM crystal structure in complex with NSD2-SET domain (PDB ID: 5LSU). SAM is shown as cyan sticks; (b) Crystal structure of DNA in complex with NSD2-PWWP1 domain (PDB ID: 5VC8). The key residues LYS-304, LYS-309, and LYS-312 in NSD2-PWWP1 domain that form direct electrostatic interactions with the DNA phosphate backbone are shown as cyan sticks; and (c) The structures of three NSD2 isoforms (NSD2-long, NSD2-short, and RE-IIBP) that are composed of multiple domains, including PWWP domain, PHD domain, SET domain (AWS/pre-SET, SET, and post-SET), etc.

Techniques:

(a) Crystal structure of compound 51 (MRT866) in complex with NSD2-PWWP1 domain (PDB ID: 7MDN). Red dash lines highlight the hydrogen bonds between compound 51 and the key residues in NSD2-PWWP1 domain. Compound 51 is shown as yellow sticks. Key residues ALA-270, GLN-321, TYR-233, TRP-236, and PHE-266 in the NSD2-PWWP1 domain are shown as green sticks. (b) Crystal structure of compound 14 (UNC6934) in complex with NSD2-PWWP1 domain (PDB ID: 6XCG). Red dash lines highlight the hydrogen bonds formed between compound 14 and the key residues in NSD2-PWWP1 domain. Compound 14 is shown as yellow sticks. Key residues ALA-270, GLN-321, TYR-233, ARG-273, TRP-236, and PHE-266 in the NSD2-PWWP1 domain are shown as green sticks.

Journal: Journal of medicinal chemistry

Article Title: Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2)

doi: 10.1021/acs.jmedchem.3c00948

Figure Lengend Snippet: (a) Crystal structure of compound 51 (MRT866) in complex with NSD2-PWWP1 domain (PDB ID: 7MDN). Red dash lines highlight the hydrogen bonds between compound 51 and the key residues in NSD2-PWWP1 domain. Compound 51 is shown as yellow sticks. Key residues ALA-270, GLN-321, TYR-233, TRP-236, and PHE-266 in the NSD2-PWWP1 domain are shown as green sticks. (b) Crystal structure of compound 14 (UNC6934) in complex with NSD2-PWWP1 domain (PDB ID: 6XCG). Red dash lines highlight the hydrogen bonds formed between compound 14 and the key residues in NSD2-PWWP1 domain. Compound 14 is shown as yellow sticks. Key residues ALA-270, GLN-321, TYR-233, ARG-273, TRP-236, and PHE-266 in the NSD2-PWWP1 domain are shown as green sticks.

Techniques:

Crystal structure of compound 54 in complex with NSD2-PWWP1 domain (PDB ID: 7VLN). Hydrogen bonds formed between compound 54 and the key residues in the NSD2-PWWP1 domain are highlighted by red dashed lines. Compound 54 is shown as yellow sticks. Key residues ALA-270, ASP-269, TYR-233, GLU-291, and GLU-272 in the NSD2-PWWP1 domain are shown as green sticks.

Journal: Journal of medicinal chemistry

Article Title: Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2)

doi: 10.1021/acs.jmedchem.3c00948

Figure Lengend Snippet: Crystal structure of compound 54 in complex with NSD2-PWWP1 domain (PDB ID: 7VLN). Hydrogen bonds formed between compound 54 and the key residues in the NSD2-PWWP1 domain are highlighted by red dashed lines. Compound 54 is shown as yellow sticks. Key residues ALA-270, ASP-269, TYR-233, GLU-291, and GLU-272 in the NSD2-PWWP1 domain are shown as green sticks.

Techniques:

Crystal structure of compound 14 (UNC6934) in complex with NSD2-PWWP1 domain (PDB ID: 6XCG). Compound 14 is shown as green sticks, and the red dashed circle highlights the pyrimidine ring that points into the solvent-exposed region.

Journal: Journal of medicinal chemistry

Article Title: Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2)

doi: 10.1021/acs.jmedchem.3c00948

Figure Lengend Snippet: Crystal structure of compound 14 (UNC6934) in complex with NSD2-PWWP1 domain (PDB ID: 6XCG). Compound 14 is shown as green sticks, and the red dashed circle highlights the pyrimidine ring that points into the solvent-exposed region.

Techniques: Solvent

A. Cell surface capture proteomics of myeloma (AMO-1 and MM.1S) cell lines in comparison to acute myeloid leukemia (AML) cell lines indicated surface expression of CD70. Re-analysis of primary patient sample surface proteomic datasets (NatComm = Ferguson et al, Nature Communications (2022); Blood = Anderson et al, Blood (2022)) also indicates detectable CD70 in some samples. Plot shows normalized abundance based on mass spectrometric intensity. B. Example mass spectra from MM.1S cell line demonstrating peptides from CD70 identified by cell surface proteomics. C. CoMMpass transcript data ( n = 776) demonstrating CD70 expression as a function of Revised International Staging System (R-ISS) stage (1, 2, 3) at diagnosis. D. Box plot of NSD2 (left) and CD70 (right) expression grouped by gene expression subtype in newly diagnosed multiple myeloma (NDMM) CoMMpass samples ( n = 764). Gene expression subtypes are from Zhan et al. (CD-1: Cyclin D1; CD-2: Cyclin D1 and CD20; HP: Hyperdiploid; LB: Low Bone Disease; MF: MAF; MS: MMSET; PR: Proliferation) E. Volcano plot of genes associated with CD70 expression in CoMMpass NDMM samples ( n = 764). Genes significantly associated with CD70 (FDR <0.01) are shown in red (positive) and blue (negative) with the numbers listed above and select genes labelled. F. Top Gene Set Enrichment Analysis (GSEA) Hallmark pathways associated with CD70 expression. Top 5 pathways positively (red) and negatively (blue) associated with CD70 expression are shown, and only pathways with an FDR < 0.01 are included. G. Top GSEA positional gene sets associated with CD70 expression. Only the top 5 pathways positively and negatively associated with CD70 expression are shown.

Journal: bioRxiv

Article Title: Targeting high-risk multiple myeloma genotypes with optimized anti-CD70 CAR-T cells

doi: 10.1101/2024.02.24.581875

Figure Lengend Snippet: A. Cell surface capture proteomics of myeloma (AMO-1 and MM.1S) cell lines in comparison to acute myeloid leukemia (AML) cell lines indicated surface expression of CD70. Re-analysis of primary patient sample surface proteomic datasets (NatComm = Ferguson et al, Nature Communications (2022); Blood = Anderson et al, Blood (2022)) also indicates detectable CD70 in some samples. Plot shows normalized abundance based on mass spectrometric intensity. B. Example mass spectra from MM.1S cell line demonstrating peptides from CD70 identified by cell surface proteomics. C. CoMMpass transcript data ( n = 776) demonstrating CD70 expression as a function of Revised International Staging System (R-ISS) stage (1, 2, 3) at diagnosis. D. Box plot of NSD2 (left) and CD70 (right) expression grouped by gene expression subtype in newly diagnosed multiple myeloma (NDMM) CoMMpass samples ( n = 764). Gene expression subtypes are from Zhan et al. (CD-1: Cyclin D1; CD-2: Cyclin D1 and CD20; HP: Hyperdiploid; LB: Low Bone Disease; MF: MAF; MS: MMSET; PR: Proliferation) E. Volcano plot of genes associated with CD70 expression in CoMMpass NDMM samples ( n = 764). Genes significantly associated with CD70 (FDR <0.01) are shown in red (positive) and blue (negative) with the numbers listed above and select genes labelled. F. Top Gene Set Enrichment Analysis (GSEA) Hallmark pathways associated with CD70 expression. Top 5 pathways positively (red) and negatively (blue) associated with CD70 expression are shown, and only pathways with an FDR < 0.01 are included. G. Top GSEA positional gene sets associated with CD70 expression. Only the top 5 pathways positively and negatively associated with CD70 expression are shown.

Article Snippet: Primary antibodies targeting NSD2 (Abcam Cat# ab75359), HDAC2 (Millipore Cat# 05-814), H3 (Cell Signaling Technology Cat# 14269) and H3K36me2 (Abcam Cat# ab9049) were diluted in blocking buffer at 1:1000.

Techniques: Comparison, Expressing

A. Knockout of the driver oncogene NSD2 in t(4;14) myeloma cell lines KMS-11 and KMS-34 led to decreased surface CD70 expression by flow cytometry. n = 3 biological replicates. p -value by t -test. *p<0.05, **p<0.01. B. MM.1S or AMO.1 myeloma cells were treated with the indicated dose of azacytidine or 0.1% DMSO for 4 days, and surface CD70 assessed by flow cytometry 3 days later. p -value by 2-way ANOVA. * p <0.05, ** p <0.01. n = 3 technical replicates. C. An eXtreme Gradient Boosting (XGB) model (see Methods) extracts features of transcription factor gene expression from CoMMpass ( n = 776) that best-model CD70 expression in patient tumors. 80% of data was used as a test set with 20% left out as a training set, with subsequent 5-fold cross validation (see Methods). n = 776 total samples included in the analysis. R 2 value corresponds to Pearson correlation between model-predicted CD70 expression in the test set and measured tumor CD70 expression in CoMMpass. D. Shapley Additive Explanations (SHAP) analysis suggest expression of transcription factors most strongly impacting CD70 expression levels in CoMMpass tumors. E. Correlation of CD70 with TFAP2A and PAX5 in the CoMMpass dataset. F. Surface CD70 by flow cytometry on LP-1 cells measured after Cas9 RNP nucleofection with sgRNA targeting TFAP2A , CD70 , or scramble control. Flow cytometry mean fluorescence intensity shown as fold-change versus isotype control. p -value by t -test. *** p <0.005, ****p<0.001. n = 3 technical replicates, representative of 2 biological replicates. Mean +/− S.D. shown.

Journal: bioRxiv

Article Title: Targeting high-risk multiple myeloma genotypes with optimized anti-CD70 CAR-T cells

doi: 10.1101/2024.02.24.581875

Figure Lengend Snippet: A. Knockout of the driver oncogene NSD2 in t(4;14) myeloma cell lines KMS-11 and KMS-34 led to decreased surface CD70 expression by flow cytometry. n = 3 biological replicates. p -value by t -test. *p<0.05, **p<0.01. B. MM.1S or AMO.1 myeloma cells were treated with the indicated dose of azacytidine or 0.1% DMSO for 4 days, and surface CD70 assessed by flow cytometry 3 days later. p -value by 2-way ANOVA. * p <0.05, ** p <0.01. n = 3 technical replicates. C. An eXtreme Gradient Boosting (XGB) model (see Methods) extracts features of transcription factor gene expression from CoMMpass ( n = 776) that best-model CD70 expression in patient tumors. 80% of data was used as a test set with 20% left out as a training set, with subsequent 5-fold cross validation (see Methods). n = 776 total samples included in the analysis. R 2 value corresponds to Pearson correlation between model-predicted CD70 expression in the test set and measured tumor CD70 expression in CoMMpass. D. Shapley Additive Explanations (SHAP) analysis suggest expression of transcription factors most strongly impacting CD70 expression levels in CoMMpass tumors. E. Correlation of CD70 with TFAP2A and PAX5 in the CoMMpass dataset. F. Surface CD70 by flow cytometry on LP-1 cells measured after Cas9 RNP nucleofection with sgRNA targeting TFAP2A , CD70 , or scramble control. Flow cytometry mean fluorescence intensity shown as fold-change versus isotype control. p -value by t -test. *** p <0.005, ****p<0.001. n = 3 technical replicates, representative of 2 biological replicates. Mean +/− S.D. shown.

Techniques: Knock-Out, Expressing, Flow Cytometry, Fluorescence

A. Immunoblots confirming NSD2 knockout in KMS11 and KMS34 cell lines. H3K36me2 signal decrease confirms functional loss of histone methylation in the context of NSD2 loss. Total HDAC2 and Histone H3 levels are unchanged. B. Called peaks from ATAC-seq (data from Jin et al (2018) at the CD70 locus, across normal memory B-cells (MB), plasmablasts, normal plasma cells, and malignant plasma cells derived from multiple myeloma (MM) patients (ten illustrated here; 24 total included in study). Dashed red lines highlight major ATAC-seq peak present only in myeloma patient samples. Transcription factor motifs (listed in ) extracted from this peak.

Journal: bioRxiv

Article Title: Targeting high-risk multiple myeloma genotypes with optimized anti-CD70 CAR-T cells

doi: 10.1101/2024.02.24.581875

Figure Lengend Snippet: A. Immunoblots confirming NSD2 knockout in KMS11 and KMS34 cell lines. H3K36me2 signal decrease confirms functional loss of histone methylation in the context of NSD2 loss. Total HDAC2 and Histone H3 levels are unchanged. B. Called peaks from ATAC-seq (data from Jin et al (2018) at the CD70 locus, across normal memory B-cells (MB), plasmablasts, normal plasma cells, and malignant plasma cells derived from multiple myeloma (MM) patients (ten illustrated here; 24 total included in study). Dashed red lines highlight major ATAC-seq peak present only in myeloma patient samples. Transcription factor motifs (listed in ) extracted from this peak.

Techniques: Western Blot, Knock-Out, Functional Assay, Methylation, Derivative Assay

All Primers for qRT-PCR of NSD2 and GAPDH

Journal: Cancer Management and Research

Article Title: NSD2 Promotes Renal Cancer Progression Through Stimulating Akt/Erk Signaling

doi: 10.2147/CMAR.S222673

Figure Lengend Snippet: All Primers for qRT-PCR of NSD2 and GAPDH

Article Snippet: The small interfering RNA targeting NSD2 (siNSD2) and negative control (siNC) were synthesized by GenePharma Company (Shanghai, China).

Techniques: Negative Control

NSD2 expression and impact on diagnosis and outcome of patients with ccRCC. ( A, B ) NSD2 expression is up-regulated in ccRCC samples (N=72) compared with paired adjacent normal samples (N=72) from the GSE53757 database (p<0.0001). ( C ) ROC curve analysis using NSD2 expression in ccRCC samples and normal samples (AUC=0.9026, p<0.0001). ( D ) NSD2 expression is negatively correlated with overall survival (OS) time in ccRCC cases from OncoLnc (N=522, p<0.0001). Abbreviations: ccRCC, clear cell renal cell carcinoma; ROC, receiver operating characteristic; AUC, area under ROC curve.

Journal: Cancer Management and Research

Article Title: NSD2 Promotes Renal Cancer Progression Through Stimulating Akt/Erk Signaling

doi: 10.2147/CMAR.S222673

Figure Lengend Snippet: NSD2 expression and impact on diagnosis and outcome of patients with ccRCC. ( A, B ) NSD2 expression is up-regulated in ccRCC samples (N=72) compared with paired adjacent normal samples (N=72) from the GSE53757 database (p<0.0001). ( C ) ROC curve analysis using NSD2 expression in ccRCC samples and normal samples (AUC=0.9026, p<0.0001). ( D ) NSD2 expression is negatively correlated with overall survival (OS) time in ccRCC cases from OncoLnc (N=522, p<0.0001). Abbreviations: ccRCC, clear cell renal cell carcinoma; ROC, receiver operating characteristic; AUC, area under ROC curve.

Article Snippet: The small interfering RNA targeting NSD2 (siNSD2) and negative control (siNC) were synthesized by GenePharma Company (Shanghai, China).

Techniques: Expressing, Biomarker Discovery

NSD2 is over-expressed in ccRCC tissues by immunohistochemistry (IHC). ( A–D ) IHC staining (4-grade score 0, +1, +2, +3) for NSD2 protein in ccRCC tissues and adjacent normal tissues. ( E ) NSD2 protein level in ccRCC specimens was higher than in normal specimens (*p=0.0003; Mann–Whitney U -test).

Journal: Cancer Management and Research

Article Title: NSD2 Promotes Renal Cancer Progression Through Stimulating Akt/Erk Signaling

doi: 10.2147/CMAR.S222673

Figure Lengend Snippet: NSD2 is over-expressed in ccRCC tissues by immunohistochemistry (IHC). ( A–D ) IHC staining (4-grade score 0, +1, +2, +3) for NSD2 protein in ccRCC tissues and adjacent normal tissues. ( E ) NSD2 protein level in ccRCC specimens was higher than in normal specimens (*p=0.0003; Mann–Whitney U -test).

Article Snippet: The small interfering RNA targeting NSD2 (siNSD2) and negative control (siNC) were synthesized by GenePharma Company (Shanghai, China).

Techniques: Immunohistochemistry, MANN-WHITNEY

NSD2 expression is elevated in ccRCC cell lines. ( A ) The expression of NSD2 mRNA is increased in three-ccRCC cell lines (786-O, ACHN and Caki-1) compared with normal cortex/proximal tubule epithelial cell line (HK-2). ( B ) The protein level of NSD2 is up-regulated in two-ccRCC cell lines (786-O and ACHN), but not obviously altered in Caki-1 cells. ( C, D ) The knockdown efficiency of siNSD2 is confirmed by qRT-PCR and Western blotting in 786-O and ACHN cells. ( E, F ) The transfection efficiency of cDNA is confirmed in Caki-1 cells. *p<0.05, n.s. p>0.05. Abbreviations: NC, negative control; qRT-PCR, quantitative real-time polymerase chain reaction; n.s., no statistical significance.

Journal: Cancer Management and Research

Article Title: NSD2 Promotes Renal Cancer Progression Through Stimulating Akt/Erk Signaling

doi: 10.2147/CMAR.S222673

Figure Lengend Snippet: NSD2 expression is elevated in ccRCC cell lines. ( A ) The expression of NSD2 mRNA is increased in three-ccRCC cell lines (786-O, ACHN and Caki-1) compared with normal cortex/proximal tubule epithelial cell line (HK-2). ( B ) The protein level of NSD2 is up-regulated in two-ccRCC cell lines (786-O and ACHN), but not obviously altered in Caki-1 cells. ( C, D ) The knockdown efficiency of siNSD2 is confirmed by qRT-PCR and Western blotting in 786-O and ACHN cells. ( E, F ) The transfection efficiency of cDNA is confirmed in Caki-1 cells. *p<0.05, n.s. p>0.05. Abbreviations: NC, negative control; qRT-PCR, quantitative real-time polymerase chain reaction; n.s., no statistical significance.

Article Snippet: The small interfering RNA targeting NSD2 (siNSD2) and negative control (siNC) were synthesized by GenePharma Company (Shanghai, China).

Techniques: Expressing, Knockdown, Quantitative RT-PCR, Western Blot, Transfection, Negative Control, Real-time Polymerase Chain Reaction

NSD2 promotes proliferation and inhibits apoptosis in ccRCC cells. ( A ) Down-regulation of NSD2 reduces cell viability of 786-O and ACHN cells. ( B ) Suppression of NSD2 induces cell apoptosis of 786-O and ACHN cells. ( C-D ) Elevation of NSD2 promotes proliferation and inhibit apoptosis in Caki-1 cells. *p<0.05. Abbreviations: MTT, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide; FITC, fluorescein isothiocyanate; PI, propidium iodide.

Journal: Cancer Management and Research

Article Title: NSD2 Promotes Renal Cancer Progression Through Stimulating Akt/Erk Signaling

doi: 10.2147/CMAR.S222673

Figure Lengend Snippet: NSD2 promotes proliferation and inhibits apoptosis in ccRCC cells. ( A ) Down-regulation of NSD2 reduces cell viability of 786-O and ACHN cells. ( B ) Suppression of NSD2 induces cell apoptosis of 786-O and ACHN cells. ( C-D ) Elevation of NSD2 promotes proliferation and inhibit apoptosis in Caki-1 cells. *p<0.05. Abbreviations: MTT, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide; FITC, fluorescein isothiocyanate; PI, propidium iodide.

Article Snippet: The small interfering RNA targeting NSD2 (siNSD2) and negative control (siNC) were synthesized by GenePharma Company (Shanghai, China).

Techniques:

NSD2 activates Akt/Erk signaling and regulates Bcl-2 and Bax expression. ( A ) Silencing of NSD2 represses p-Akt, p-Erk1/2, Bcl-2 expression, and enhances Bax expression, but not alters total Akt and Erk1/2 expression in 786-O and ACHN cells. ( B ) Over-expression of NSD2 increases p-Akt, p-Erk1/2 and Bcl-2 protein, and decreases Bax protein in Caki-1 cells. *p<0.05. Abbreviations: p-Akt, phospho-Akt; p-Erk1/2, phospho-Erk1/2.

Journal: Cancer Management and Research

Article Title: NSD2 Promotes Renal Cancer Progression Through Stimulating Akt/Erk Signaling

doi: 10.2147/CMAR.S222673

Figure Lengend Snippet: NSD2 activates Akt/Erk signaling and regulates Bcl-2 and Bax expression. ( A ) Silencing of NSD2 represses p-Akt, p-Erk1/2, Bcl-2 expression, and enhances Bax expression, but not alters total Akt and Erk1/2 expression in 786-O and ACHN cells. ( B ) Over-expression of NSD2 increases p-Akt, p-Erk1/2 and Bcl-2 protein, and decreases Bax protein in Caki-1 cells. *p<0.05. Abbreviations: p-Akt, phospho-Akt; p-Erk1/2, phospho-Erk1/2.

Article Snippet: The small interfering RNA targeting NSD2 (siNSD2) and negative control (siNC) were synthesized by GenePharma Company (Shanghai, China).

Techniques: Expressing, Over Expression

Knockdown of NSD2 reduces the formation of xenograft tumors in vivo. ( A ) The fluorescence microscope is used to detect the efficiency of LV-shNC and LV-shNSD2 transfection. ( B ) Subcutaneous tumors formed in nude mice by 786-O cells stably inhibition of NSD2 or control. ( C ) Tumor formation growth curves after injection of transfected cells. ( D ) The mean tumor weights of each group. *p<0.05. Abbreviation: LV, lentiviral vector.

Journal: Cancer Management and Research

Article Title: NSD2 Promotes Renal Cancer Progression Through Stimulating Akt/Erk Signaling

doi: 10.2147/CMAR.S222673

Figure Lengend Snippet: Knockdown of NSD2 reduces the formation of xenograft tumors in vivo. ( A ) The fluorescence microscope is used to detect the efficiency of LV-shNC and LV-shNSD2 transfection. ( B ) Subcutaneous tumors formed in nude mice by 786-O cells stably inhibition of NSD2 or control. ( C ) Tumor formation growth curves after injection of transfected cells. ( D ) The mean tumor weights of each group. *p<0.05. Abbreviation: LV, lentiviral vector.

Article Snippet: The small interfering RNA targeting NSD2 (siNSD2) and negative control (siNC) were synthesized by GenePharma Company (Shanghai, China).

Techniques: Knockdown, In Vivo, Fluorescence, Microscopy, Transfection, Stable Transfection, Inhibition, Control, Injection, Plasmid Preparation

Journal: International Journal of Medical Sciences

Article Title: Knockdown of NSD2 Suppresses Renal Cell Carcinoma Metastasis by Inhibiting Epithelial-Mesenchymal Transition

doi: 10.7150/ijms.36128

Figure Lengend Snippet: All primers for qRT-PCR of NSD2 and GAPDH.

Article Snippet: Three small interfering RNAs (siRNAs) targeting NSD2 were synthesized by GenePharma Company (Shanghai, China).

Techniques: Negative Control

NSD2 was up-regulated in renal cancer samples. (A) NSD2 mRNA expression was elevated in several types of renal cancer and NSD2 was highly expressed in ccRCC (P < 0.0001). (B) The expression of NSD2 mRNA was obviously higher in primary ccRCC samples (P < 0.0001) and metastatic ccRCC samples (P = 0.0002). Besides, NSD2 mRNA in primary ccRCC expressed lower than in metastatic ccRCC (P = 0.0328).

Journal: International Journal of Medical Sciences

Article Title: Knockdown of NSD2 Suppresses Renal Cell Carcinoma Metastasis by Inhibiting Epithelial-Mesenchymal Transition

doi: 10.7150/ijms.36128

Figure Lengend Snippet: NSD2 was up-regulated in renal cancer samples. (A) NSD2 mRNA expression was elevated in several types of renal cancer and NSD2 was highly expressed in ccRCC (P < 0.0001). (B) The expression of NSD2 mRNA was obviously higher in primary ccRCC samples (P < 0.0001) and metastatic ccRCC samples (P = 0.0002). Besides, NSD2 mRNA in primary ccRCC expressed lower than in metastatic ccRCC (P = 0.0328).

Article Snippet: Three small interfering RNAs (siRNAs) targeting NSD2 were synthesized by GenePharma Company (Shanghai, China).

Techniques: Expressing

NSD2 was over-expressed in ccRCC tissues by immunohistochemistry (IHC). (A) IHC staining (3-grade score 0, +1, +2) for NSD2 in tissue microarrays of patients with locoregionally advanced ccRCC or normal epithelium. (B) NSD2 protein level was higher both in low grade and high grade ccRCC tissues than in normal tissues (P = 0.0483; P = 0.0221; Mann-Whitney U test). But the difference between low grade and high grade was not significant (P = 0.5513; Mann-Whitney U test). (C) High NSD2 protein level did not correlate with high grade in ccRCC tissues (P = 0.6942; Fisher exact test).

Journal: International Journal of Medical Sciences

Article Title: Knockdown of NSD2 Suppresses Renal Cell Carcinoma Metastasis by Inhibiting Epithelial-Mesenchymal Transition

doi: 10.7150/ijms.36128

Figure Lengend Snippet: NSD2 was over-expressed in ccRCC tissues by immunohistochemistry (IHC). (A) IHC staining (3-grade score 0, +1, +2) for NSD2 in tissue microarrays of patients with locoregionally advanced ccRCC or normal epithelium. (B) NSD2 protein level was higher both in low grade and high grade ccRCC tissues than in normal tissues (P = 0.0483; P = 0.0221; Mann-Whitney U test). But the difference between low grade and high grade was not significant (P = 0.5513; Mann-Whitney U test). (C) High NSD2 protein level did not correlate with high grade in ccRCC tissues (P = 0.6942; Fisher exact test).

Article Snippet: Three small interfering RNAs (siRNAs) targeting NSD2 were synthesized by GenePharma Company (Shanghai, China).

Techniques: Immunohistochemistry, MANN-WHITNEY

NSD2 was effectively knocked down by siRNAs in RCC cells. (A) The expression of NSD2 mRNA was potently suppressed by different siRNAs in 786-O and ACHN cells. (B) The expression of NSD2 protein was strikingly diminished by siNSD2#2 in 786-O and ACHN cells. (*, P < 0.05)

Journal: International Journal of Medical Sciences

Article Title: Knockdown of NSD2 Suppresses Renal Cell Carcinoma Metastasis by Inhibiting Epithelial-Mesenchymal Transition

doi: 10.7150/ijms.36128

Figure Lengend Snippet: NSD2 was effectively knocked down by siRNAs in RCC cells. (A) The expression of NSD2 mRNA was potently suppressed by different siRNAs in 786-O and ACHN cells. (B) The expression of NSD2 protein was strikingly diminished by siNSD2#2 in 786-O and ACHN cells. (*, P < 0.05)

Article Snippet: Three small interfering RNAs (siRNAs) targeting NSD2 were synthesized by GenePharma Company (Shanghai, China).

Techniques: Expressing

Depletion of NSD2 inhibited cell migration and invasion in RCC. (A) Down-regulation of NSD2 reduced migratory properties in 786-O and ACHN cells. (B) Sliencing of NSD2 repressed invasive properties in 786-O and ACHN cells. (*, P < 0.05)

Journal: International Journal of Medical Sciences

Article Title: Knockdown of NSD2 Suppresses Renal Cell Carcinoma Metastasis by Inhibiting Epithelial-Mesenchymal Transition

doi: 10.7150/ijms.36128

Figure Lengend Snippet: Depletion of NSD2 inhibited cell migration and invasion in RCC. (A) Down-regulation of NSD2 reduced migratory properties in 786-O and ACHN cells. (B) Sliencing of NSD2 repressed invasive properties in 786-O and ACHN cells. (*, P < 0.05)

Article Snippet: Three small interfering RNAs (siRNAs) targeting NSD2 were synthesized by GenePharma Company (Shanghai, China).

Techniques: Migration

NSD2 regulated epithelial-mesenchymal transition (EMT). Inhibition of NSD2 increased the expression of E-cadherin protein and decreased the expressions of N-cadherin and Vimentin protein in 786-O and ACHN cells. (*, P < 0.05)

Journal: International Journal of Medical Sciences

Article Title: Knockdown of NSD2 Suppresses Renal Cell Carcinoma Metastasis by Inhibiting Epithelial-Mesenchymal Transition

doi: 10.7150/ijms.36128

Figure Lengend Snippet: NSD2 regulated epithelial-mesenchymal transition (EMT). Inhibition of NSD2 increased the expression of E-cadherin protein and decreased the expressions of N-cadherin and Vimentin protein in 786-O and ACHN cells. (*, P < 0.05)

Article Snippet: Three small interfering RNAs (siRNAs) targeting NSD2 were synthesized by GenePharma Company (Shanghai, China).

Techniques: Inhibition, Expressing

The relationship between NSD2 expression and clinicopathological parameters of ccRCC patients.

Journal: International Journal of Medical Sciences

Article Title: Knockdown of NSD2 Suppresses Renal Cell Carcinoma Metastasis by Inhibiting Epithelial-Mesenchymal Transition

doi: 10.7150/ijms.36128

Figure Lengend Snippet: The relationship between NSD2 expression and clinicopathological parameters of ccRCC patients.

Article Snippet: Three small interfering RNAs (siRNAs) targeting NSD2 were synthesized by GenePharma Company (Shanghai, China).

Techniques: Expressing

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