normal tissue data Search Results


pdac tissue array  (AMS Biotechnology)
86
AMS Biotechnology pdac tissue array
Figure 8: <t>PDAC</t> tumor tissue array show enhanced expression of ADAM10: A.-C. Tumor tissue array containing normal, islet cell tumor and Grade I, II and III <t>PDAC</t> <t>tissue</t> samples were immunostained using an ADAM10 antibody A. and intensity of the stained sections were measured by Dr. Coppola, Senior Pathologist at Moffitt Cancer Center. The stain was semiquantitatively scored based on the intensity of the stain as negative (0), weak (1), moderate (2) and strong (3). In all cases at least 34% of the tumor was positive, which is shown in B. The bargraph in C. shows that ADAM10 levels are increased in tumor tissues, with Grade 1 tumors showing a significant increase. D.-J. Expression of vimentin, c-Myc and ADAM10 are significantly increased in PDAC: PDAC tissue samples and samples from normal pancreas were analyzed by western blot using vimentin (D. and H.), c-Myc (E. and I.) and ADAM10 (F. and J.) antibodies and blots were reprobed with GAPDH antibody for normalization of proteins. K. Graph plotted using the data derived from TCGA portal show that PDAC human samples show increased alterations, especially amplification and/or mutation, in ADAM10, β-catenin (CTNNB1), cyclin D1 (CCND1), CD44, Myc (MYC) and vimentin (VIM). L. Proposed signaling mechanisms by which calcium dysregulation enhances ADAM10-mediated tumor progression: Based on our data with fendiline we hypothesize that calcium influx induces ADAM10 activation, leading to enhanced cadherin cleavage, release of β-catenin, its nuclear translocation and activation of TCF/LEF containing promoters. This enhances expression of genes associated with proliferation, epithelial mesenchymal transition and metastasis of cancers such as c-Myc, cyclin D1 and CD44. Additionally, β-catenin/TCF signaling has been shown to enhance ADAM10 expression thereby playing a feed-forward role in ADAM10-mediated downstream signaling and promotion of oncogenic cycle. In addition to this indirect activation of β-catenin-TCF signaling, ADAM10-mediated cleavage of substrates such as cadherins and CD44 allow detachment of cell-cell and cell-substratum adhesions, migration and invasion of cancer cells. Our data indicate that inhibitors of calcium channels prevent ADAM10- dependent signaling and expression of c-Myc, cyclin D1 and CD44, by stabilizing cadherin-catenin interaction at the cell membrane, enhancing adherens junction formation, subsequently reducing p-catenin-TCF/LEF signaling and target gene expression.
Pdac Tissue Array, supplied by AMS Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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normal tissue data  (Human Protein Atlas)
90
Human Protein Atlas normal tissue data
Figure 8: <t>PDAC</t> tumor tissue array show enhanced expression of ADAM10: A.-C. Tumor tissue array containing normal, islet cell tumor and Grade I, II and III <t>PDAC</t> <t>tissue</t> samples were immunostained using an ADAM10 antibody A. and intensity of the stained sections were measured by Dr. Coppola, Senior Pathologist at Moffitt Cancer Center. The stain was semiquantitatively scored based on the intensity of the stain as negative (0), weak (1), moderate (2) and strong (3). In all cases at least 34% of the tumor was positive, which is shown in B. The bargraph in C. shows that ADAM10 levels are increased in tumor tissues, with Grade 1 tumors showing a significant increase. D.-J. Expression of vimentin, c-Myc and ADAM10 are significantly increased in PDAC: PDAC tissue samples and samples from normal pancreas were analyzed by western blot using vimentin (D. and H.), c-Myc (E. and I.) and ADAM10 (F. and J.) antibodies and blots were reprobed with GAPDH antibody for normalization of proteins. K. Graph plotted using the data derived from TCGA portal show that PDAC human samples show increased alterations, especially amplification and/or mutation, in ADAM10, β-catenin (CTNNB1), cyclin D1 (CCND1), CD44, Myc (MYC) and vimentin (VIM). L. Proposed signaling mechanisms by which calcium dysregulation enhances ADAM10-mediated tumor progression: Based on our data with fendiline we hypothesize that calcium influx induces ADAM10 activation, leading to enhanced cadherin cleavage, release of β-catenin, its nuclear translocation and activation of TCF/LEF containing promoters. This enhances expression of genes associated with proliferation, epithelial mesenchymal transition and metastasis of cancers such as c-Myc, cyclin D1 and CD44. Additionally, β-catenin/TCF signaling has been shown to enhance ADAM10 expression thereby playing a feed-forward role in ADAM10-mediated downstream signaling and promotion of oncogenic cycle. In addition to this indirect activation of β-catenin-TCF signaling, ADAM10-mediated cleavage of substrates such as cadherins and CD44 allow detachment of cell-cell and cell-substratum adhesions, migration and invasion of cancer cells. Our data indicate that inhibitors of calcium channels prevent ADAM10- dependent signaling and expression of c-Myc, cyclin D1 and CD44, by stabilizing cadherin-catenin interaction at the cell membrane, enhancing adherens junction formation, subsequently reducing p-catenin-TCF/LEF signaling and target gene expression.
Normal Tissue Data, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mrna expression data for 37 different normal tissues  (Human Protein Atlas)
90
Human Protein Atlas mrna expression data for 37 different normal tissues
Figure 8: <t>PDAC</t> tumor tissue array show enhanced expression of ADAM10: A.-C. Tumor tissue array containing normal, islet cell tumor and Grade I, II and III <t>PDAC</t> <t>tissue</t> samples were immunostained using an ADAM10 antibody A. and intensity of the stained sections were measured by Dr. Coppola, Senior Pathologist at Moffitt Cancer Center. The stain was semiquantitatively scored based on the intensity of the stain as negative (0), weak (1), moderate (2) and strong (3). In all cases at least 34% of the tumor was positive, which is shown in B. The bargraph in C. shows that ADAM10 levels are increased in tumor tissues, with Grade 1 tumors showing a significant increase. D.-J. Expression of vimentin, c-Myc and ADAM10 are significantly increased in PDAC: PDAC tissue samples and samples from normal pancreas were analyzed by western blot using vimentin (D. and H.), c-Myc (E. and I.) and ADAM10 (F. and J.) antibodies and blots were reprobed with GAPDH antibody for normalization of proteins. K. Graph plotted using the data derived from TCGA portal show that PDAC human samples show increased alterations, especially amplification and/or mutation, in ADAM10, β-catenin (CTNNB1), cyclin D1 (CCND1), CD44, Myc (MYC) and vimentin (VIM). L. Proposed signaling mechanisms by which calcium dysregulation enhances ADAM10-mediated tumor progression: Based on our data with fendiline we hypothesize that calcium influx induces ADAM10 activation, leading to enhanced cadherin cleavage, release of β-catenin, its nuclear translocation and activation of TCF/LEF containing promoters. This enhances expression of genes associated with proliferation, epithelial mesenchymal transition and metastasis of cancers such as c-Myc, cyclin D1 and CD44. Additionally, β-catenin/TCF signaling has been shown to enhance ADAM10 expression thereby playing a feed-forward role in ADAM10-mediated downstream signaling and promotion of oncogenic cycle. In addition to this indirect activation of β-catenin-TCF signaling, ADAM10-mediated cleavage of substrates such as cadherins and CD44 allow detachment of cell-cell and cell-substratum adhesions, migration and invasion of cancer cells. Our data indicate that inhibitors of calcium channels prevent ADAM10- dependent signaling and expression of c-Myc, cyclin D1 and CD44, by stabilizing cadherin-catenin interaction at the cell membrane, enhancing adherens junction formation, subsequently reducing p-catenin-TCF/LEF signaling and target gene expression.
Mrna Expression Data For 37 Different Normal Tissues, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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immunohistochemistry (ihc) data for prad and normal prostate tissues  (Human Protein Atlas)
90
Human Protein Atlas immunohistochemistry (ihc) data for prad and normal prostate tissues
Figure 8: <t>PDAC</t> tumor tissue array show enhanced expression of ADAM10: A.-C. Tumor tissue array containing normal, islet cell tumor and Grade I, II and III <t>PDAC</t> <t>tissue</t> samples were immunostained using an ADAM10 antibody A. and intensity of the stained sections were measured by Dr. Coppola, Senior Pathologist at Moffitt Cancer Center. The stain was semiquantitatively scored based on the intensity of the stain as negative (0), weak (1), moderate (2) and strong (3). In all cases at least 34% of the tumor was positive, which is shown in B. The bargraph in C. shows that ADAM10 levels are increased in tumor tissues, with Grade 1 tumors showing a significant increase. D.-J. Expression of vimentin, c-Myc and ADAM10 are significantly increased in PDAC: PDAC tissue samples and samples from normal pancreas were analyzed by western blot using vimentin (D. and H.), c-Myc (E. and I.) and ADAM10 (F. and J.) antibodies and blots were reprobed with GAPDH antibody for normalization of proteins. K. Graph plotted using the data derived from TCGA portal show that PDAC human samples show increased alterations, especially amplification and/or mutation, in ADAM10, β-catenin (CTNNB1), cyclin D1 (CCND1), CD44, Myc (MYC) and vimentin (VIM). L. Proposed signaling mechanisms by which calcium dysregulation enhances ADAM10-mediated tumor progression: Based on our data with fendiline we hypothesize that calcium influx induces ADAM10 activation, leading to enhanced cadherin cleavage, release of β-catenin, its nuclear translocation and activation of TCF/LEF containing promoters. This enhances expression of genes associated with proliferation, epithelial mesenchymal transition and metastasis of cancers such as c-Myc, cyclin D1 and CD44. Additionally, β-catenin/TCF signaling has been shown to enhance ADAM10 expression thereby playing a feed-forward role in ADAM10-mediated downstream signaling and promotion of oncogenic cycle. In addition to this indirect activation of β-catenin-TCF signaling, ADAM10-mediated cleavage of substrates such as cadherins and CD44 allow detachment of cell-cell and cell-substratum adhesions, migration and invasion of cancer cells. Our data indicate that inhibitors of calcium channels prevent ADAM10- dependent signaling and expression of c-Myc, cyclin D1 and CD44, by stabilizing cadherin-catenin interaction at the cell membrane, enhancing adherens junction formation, subsequently reducing p-catenin-TCF/LEF signaling and target gene expression.
Immunohistochemistry (Ihc) Data For Prad And Normal Prostate Tissues, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mrna expression data of tgif2 in normal tissues  (Human Protein Atlas)
90
Human Protein Atlas mrna expression data of tgif2 in normal tissues
The expression level of <t>TGIF2</t> in different human cancers and its relationship to glioma prognosis. (A) TGIF2 mRNA expression across various human organs and tissues based on consensus dataset in HPA database. (B) Comparison of TGIF2 expression between normal and tumor tissues across 33 cancers in TCGA and the GTEx database. (C) Subcellular localization of TGIF2 in SH-SY5Y cells from HPA datasets. (D) The volcano plot of DEGs in GSE14805. Red points represent upregulated, blue points represents downregulated genes. (E) ROC curve of TGIF2 and other established prognostic genes (IDH1, IDH2, EGFR, TP53, CDC6, CDC14B, CHD5) in glioma. (F–H) Survival curves for OS (F) , DSS (G) and PFI (H) in gliomas using TCGA database. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
Mrna Expression Data Of Tgif2 In Normal Tissues, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ddb2 expression data in normal tongue tissues, tongue sccs, normal larynx and larynx sccs  (U.S Biomax Inc)
90
U.S Biomax Inc ddb2 expression data in normal tongue tissues, tongue sccs, normal larynx and larynx sccs
( A ) A representative Kaplan–Meier analysis of overall survival of HNSCC patients ( n = 81) stratified according <t>to</t> <t>DDB2</t> expression in tumors. Patients with higher DDB2 expression survived longer compared to patients with lower DDB2 expression, significant at alpha level of 0.05 (log rank p = 0.0404). ( B ) Loss of DDB2 expression in HNSCCs. DDB2-immunohistochemistry of human tissue microarrays (US Biomax # HN242a and HN811a). Representative images from normal tongue tissue, tongue <t>SCCs</t> of grades 1–3 stage I–III and cancer adjacent normal tongue tissue (NAT), normal larynx tissues and larynx SCCs grade 2 stage III and IV are shown. Scale bar for all the images, 10 μm. ( C ) The average intensity of DDB2 staining of normal tongue versus tongue SCCs showed lower staining in all SCC tissues and acute loss of staining in advanced SCCs. p < 0.0001.
Ddb2 Expression Data In Normal Tongue Tissues, Tongue Sccs, Normal Larynx And Larynx Sccs, supplied by U.S Biomax Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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normal tissue fpkm data  (Human Protein Atlas)
90
Human Protein Atlas normal tissue fpkm data
( A ) A representative Kaplan–Meier analysis of overall survival of HNSCC patients ( n = 81) stratified according <t>to</t> <t>DDB2</t> expression in tumors. Patients with higher DDB2 expression survived longer compared to patients with lower DDB2 expression, significant at alpha level of 0.05 (log rank p = 0.0404). ( B ) Loss of DDB2 expression in HNSCCs. DDB2-immunohistochemistry of human tissue microarrays (US Biomax # HN242a and HN811a). Representative images from normal tongue tissue, tongue <t>SCCs</t> of grades 1–3 stage I–III and cancer adjacent normal tongue tissue (NAT), normal larynx tissues and larynx SCCs grade 2 stage III and IV are shown. Scale bar for all the images, 10 μm. ( C ) The average intensity of DDB2 staining of normal tongue versus tongue SCCs showed lower staining in all SCC tissues and acute loss of staining in advanced SCCs. p < 0.0001.
Normal Tissue Fpkm Data, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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hcc and normal liver tissues expression data  (Human Protein Atlas)
90
Human Protein Atlas hcc and normal liver tissues expression data
Mutational landscape of <t>SMGs</t> <t>in</t> <t>HCC.</t> (A) Significantly mutated genes in HCC. The different colors represent different mutation types. (B) Expression of SMGs in HCC and normal tissues. According to an analysis of immunohistochemical staining data from the Human Protein Atlas database, the expression of SMGs in HCC was compared with that in normal tissues.
Hcc And Normal Liver Tissues Expression Data, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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normal tissue scrnaseq data  (Human Protein Atlas)
90
Human Protein Atlas normal tissue scrnaseq data
Mutational landscape of <t>SMGs</t> <t>in</t> <t>HCC.</t> (A) Significantly mutated genes in HCC. The different colors represent different mutation types. (B) Expression of SMGs in HCC and normal tissues. According to an analysis of immunohistochemical staining data from the Human Protein Atlas database, the expression of SMGs in HCC was compared with that in normal tissues.
Normal Tissue Scrnaseq Data, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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poly(a)+ rna-seq data for normal healthy tissues  (Broad Institute Inc)
90
Broad Institute Inc poly(a)+ rna-seq data for normal healthy tissues
Mutational landscape of <t>SMGs</t> <t>in</t> <t>HCC.</t> (A) Significantly mutated genes in HCC. The different colors represent different mutation types. (B) Expression of SMGs in HCC and normal tissues. According to an analysis of immunohistochemical staining data from the Human Protein Atlas database, the expression of SMGs in HCC was compared with that in normal tissues.
Poly(A)+ Rna Seq Data For Normal Healthy Tissues, supplied by Broad Institute Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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super-sage data for malat1 expression in pancreas carcinoma and pancreatitis compared to normal pancreas tissue  (GenXPro Inc)
90
GenXPro Inc super-sage data for malat1 expression in pancreas carcinoma and pancreatitis compared to normal pancreas tissue
Mutational landscape of <t>SMGs</t> <t>in</t> <t>HCC.</t> (A) Significantly mutated genes in HCC. The different colors represent different mutation types. (B) Expression of SMGs in HCC and normal tissues. According to an analysis of immunohistochemical staining data from the Human Protein Atlas database, the expression of SMGs in HCC was compared with that in normal tissues.
Super Sage Data For Malat1 Expression In Pancreas Carcinoma And Pancreatitis Compared To Normal Pancreas Tissue, supplied by GenXPro Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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normal tissue ihc data v.23.0  (Human Protein Atlas)
90
Human Protein Atlas normal tissue ihc data v.23.0
(A &B) Contingency tables used to determine the likelihood of detecting a clinical (A) ADC and (B) CAR T target in the PDX human tumor N -glycoproteome against all other surface proteins in the human proteome. P-values were calculated using a Fisher’s exact test. (C) Normal tissue toxicity scoring system. (D) Distribution of full body normal tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Jiang et al., (left), Human Protein Atlas (middle) and GTEx RNA-seq data (right). (E) Distribution of normal brain tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Tushaus et al., (left), Human Protein Atlas brain <t>IHC</t> <t>data</t> (middle) and Human Protein Atlas brain RNA-seq data (right). (F) Distribution of normal heart tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Berg Luecke et al., (left) and Doll et al., (middle & right). (D-F) P-values from unpaired Mann-Whitney U tests.
Normal Tissue Ihc Data V.23.0, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Figure 8: PDAC tumor tissue array show enhanced expression of ADAM10: A.-C. Tumor tissue array containing normal, islet cell tumor and Grade I, II and III PDAC tissue samples were immunostained using an ADAM10 antibody A. and intensity of the stained sections were measured by Dr. Coppola, Senior Pathologist at Moffitt Cancer Center. The stain was semiquantitatively scored based on the intensity of the stain as negative (0), weak (1), moderate (2) and strong (3). In all cases at least 34% of the tumor was positive, which is shown in B. The bargraph in C. shows that ADAM10 levels are increased in tumor tissues, with Grade 1 tumors showing a significant increase. D.-J. Expression of vimentin, c-Myc and ADAM10 are significantly increased in PDAC: PDAC tissue samples and samples from normal pancreas were analyzed by western blot using vimentin (D. and H.), c-Myc (E. and I.) and ADAM10 (F. and J.) antibodies and blots were reprobed with GAPDH antibody for normalization of proteins. K. Graph plotted using the data derived from TCGA portal show that PDAC human samples show increased alterations, especially amplification and/or mutation, in ADAM10, β-catenin (CTNNB1), cyclin D1 (CCND1), CD44, Myc (MYC) and vimentin (VIM). L. Proposed signaling mechanisms by which calcium dysregulation enhances ADAM10-mediated tumor progression: Based on our data with fendiline we hypothesize that calcium influx induces ADAM10 activation, leading to enhanced cadherin cleavage, release of β-catenin, its nuclear translocation and activation of TCF/LEF containing promoters. This enhances expression of genes associated with proliferation, epithelial mesenchymal transition and metastasis of cancers such as c-Myc, cyclin D1 and CD44. Additionally, β-catenin/TCF signaling has been shown to enhance ADAM10 expression thereby playing a feed-forward role in ADAM10-mediated downstream signaling and promotion of oncogenic cycle. In addition to this indirect activation of β-catenin-TCF signaling, ADAM10-mediated cleavage of substrates such as cadherins and CD44 allow detachment of cell-cell and cell-substratum adhesions, migration and invasion of cancer cells. Our data indicate that inhibitors of calcium channels prevent ADAM10- dependent signaling and expression of c-Myc, cyclin D1 and CD44, by stabilizing cadherin-catenin interaction at the cell membrane, enhancing adherens junction formation, subsequently reducing p-catenin-TCF/LEF signaling and target gene expression.

Journal: Oncotarget

Article Title: Fendiline inhibits proliferation and invasion of pancreatic cancer cells by interfering with ADAM10 activation and β-catenin signaling.

doi: 10.18632/oncotarget.5933

Figure Lengend Snippet: Figure 8: PDAC tumor tissue array show enhanced expression of ADAM10: A.-C. Tumor tissue array containing normal, islet cell tumor and Grade I, II and III PDAC tissue samples were immunostained using an ADAM10 antibody A. and intensity of the stained sections were measured by Dr. Coppola, Senior Pathologist at Moffitt Cancer Center. The stain was semiquantitatively scored based on the intensity of the stain as negative (0), weak (1), moderate (2) and strong (3). In all cases at least 34% of the tumor was positive, which is shown in B. The bargraph in C. shows that ADAM10 levels are increased in tumor tissues, with Grade 1 tumors showing a significant increase. D.-J. Expression of vimentin, c-Myc and ADAM10 are significantly increased in PDAC: PDAC tissue samples and samples from normal pancreas were analyzed by western blot using vimentin (D. and H.), c-Myc (E. and I.) and ADAM10 (F. and J.) antibodies and blots were reprobed with GAPDH antibody for normalization of proteins. K. Graph plotted using the data derived from TCGA portal show that PDAC human samples show increased alterations, especially amplification and/or mutation, in ADAM10, β-catenin (CTNNB1), cyclin D1 (CCND1), CD44, Myc (MYC) and vimentin (VIM). L. Proposed signaling mechanisms by which calcium dysregulation enhances ADAM10-mediated tumor progression: Based on our data with fendiline we hypothesize that calcium influx induces ADAM10 activation, leading to enhanced cadherin cleavage, release of β-catenin, its nuclear translocation and activation of TCF/LEF containing promoters. This enhances expression of genes associated with proliferation, epithelial mesenchymal transition and metastasis of cancers such as c-Myc, cyclin D1 and CD44. Additionally, β-catenin/TCF signaling has been shown to enhance ADAM10 expression thereby playing a feed-forward role in ADAM10-mediated downstream signaling and promotion of oncogenic cycle. In addition to this indirect activation of β-catenin-TCF signaling, ADAM10-mediated cleavage of substrates such as cadherins and CD44 allow detachment of cell-cell and cell-substratum adhesions, migration and invasion of cancer cells. Our data indicate that inhibitors of calcium channels prevent ADAM10- dependent signaling and expression of c-Myc, cyclin D1 and CD44, by stabilizing cadherin-catenin interaction at the cell membrane, enhancing adherens junction formation, subsequently reducing p-catenin-TCF/LEF signaling and target gene expression.

Article Snippet: Immunohistochemical analysis of human PDAC tissue tumor microarray The PDAC tissue array was purchased from amsbio (Cambridge, MA).

Techniques: Expressing, Staining, Western Blot, Derivative Assay, Amplification, Mutagenesis, Activation Assay, Translocation Assay, Migration, Membrane, Targeted Gene Expression

The expression level of TGIF2 in different human cancers and its relationship to glioma prognosis. (A) TGIF2 mRNA expression across various human organs and tissues based on consensus dataset in HPA database. (B) Comparison of TGIF2 expression between normal and tumor tissues across 33 cancers in TCGA and the GTEx database. (C) Subcellular localization of TGIF2 in SH-SY5Y cells from HPA datasets. (D) The volcano plot of DEGs in GSE14805. Red points represent upregulated, blue points represents downregulated genes. (E) ROC curve of TGIF2 and other established prognostic genes (IDH1, IDH2, EGFR, TP53, CDC6, CDC14B, CHD5) in glioma. (F–H) Survival curves for OS (F) , DSS (G) and PFI (H) in gliomas using TCGA database. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: The expression level of TGIF2 in different human cancers and its relationship to glioma prognosis. (A) TGIF2 mRNA expression across various human organs and tissues based on consensus dataset in HPA database. (B) Comparison of TGIF2 expression between normal and tumor tissues across 33 cancers in TCGA and the GTEx database. (C) Subcellular localization of TGIF2 in SH-SY5Y cells from HPA datasets. (D) The volcano plot of DEGs in GSE14805. Red points represent upregulated, blue points represents downregulated genes. (E) ROC curve of TGIF2 and other established prognostic genes (IDH1, IDH2, EGFR, TP53, CDC6, CDC14B, CHD5) in glioma. (F–H) Survival curves for OS (F) , DSS (G) and PFI (H) in gliomas using TCGA database. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Expressing, Comparison

Clinical characteristics of glioma patients.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Clinical characteristics of glioma patients.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques:

Logistic analysis of the association between TGIF2 expression and clinical characteristics.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Logistic analysis of the association between TGIF2 expression and clinical characteristics.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Expressing

Associations between TGIF2 expression and various clinicopathologic characteristics in glioma. (A) Age. (B) IDH status. (C) 1p/19q codeletion status. (D) Primary therapy outcome. (E) OS events. (F) DSS events. (G) PFI events. (H) WHO grade. (I) Histological type. (J) Gender. (K) Race. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ns, not significant.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Associations between TGIF2 expression and various clinicopathologic characteristics in glioma. (A) Age. (B) IDH status. (C) 1p/19q codeletion status. (D) Primary therapy outcome. (E) OS events. (F) DSS events. (G) PFI events. (H) WHO grade. (I) Histological type. (J) Gender. (K) Race. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ns, not significant.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Expressing

Prognostic value of TGIF2 expression level in glioma. (A) TGIF2 expression distribution and survival status. (B) Time-dependent ROC curves for TGIF2 expression in glioma. (C) Forest plot of OS by multivariate Cox regression analysis in glioma from TCGA database. (D) The nomogram for predicting 1-, 3-, or 5-year OS rates in patients with glioma. (E) The calibration curves for the nomogram.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Prognostic value of TGIF2 expression level in glioma. (A) TGIF2 expression distribution and survival status. (B) Time-dependent ROC curves for TGIF2 expression in glioma. (C) Forest plot of OS by multivariate Cox regression analysis in glioma from TCGA database. (D) The nomogram for predicting 1-, 3-, or 5-year OS rates in patients with glioma. (E) The calibration curves for the nomogram.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Expressing

Univariate and multivariate cox regression analyses of clinical characteristics associated with overall survival.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Univariate and multivariate cox regression analyses of clinical characteristics associated with overall survival.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques:

Correlations between TGIF2 expression level and OS in different clinicopathologic subgroups of glioma by Kaplan-Meier survival curve analysis. (A) Age ≤ 60. (B) Age > 60. (C) Gender: Male. (D) Gender: Female. (E) Race: White. (F) WHO grade: G3. (G) 1p/19q codeletion: non-codeletion. (H) Histological type: Astrocytoma. (I) Primary therapy outcome: PD.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Correlations between TGIF2 expression level and OS in different clinicopathologic subgroups of glioma by Kaplan-Meier survival curve analysis. (A) Age ≤ 60. (B) Age > 60. (C) Gender: Male. (D) Gender: Female. (E) Race: White. (F) WHO grade: G3. (G) 1p/19q codeletion: non-codeletion. (H) Histological type: Astrocytoma. (I) Primary therapy outcome: PD.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Expressing

Functional enrichment analysis of DEGs between TGIF2 high and low expression groups. (A) The volcano plot of DEGs. Red represents upregulated, blue represents downregulated genes. (B) GO and KEGG pathway enrichment analysis of DEGs. (C–H) GSEA functional enrichment analysis.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Functional enrichment analysis of DEGs between TGIF2 high and low expression groups. (A) The volcano plot of DEGs. Red represents upregulated, blue represents downregulated genes. (B) GO and KEGG pathway enrichment analysis of DEGs. (C–H) GSEA functional enrichment analysis.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Functional Assay, Expressing

Correlations between TGIF2 expression and immune cell infiltration in glioma. (A–C) Comparison of StromalScore, ImmuneScore, and EstimateScore between TGIF2 high and low expression groups. (D, E) Comparison of immune cell enrichment scores in high and low TGIF2 expression groups. (F) The lollipop chart showing the correlations between the relative abundances of 24 immune cells and TGIF2 expression levels. (G–N) Scatterplots demonstrating the positive correlation of TGIF2 expression with Th2 cells, macrophages, eosinophils, and neutrophils, and the negative correlation with mast cells, NK CD56bright cells, pDC cells, and TFH cells. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ns, not significant.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Correlations between TGIF2 expression and immune cell infiltration in glioma. (A–C) Comparison of StromalScore, ImmuneScore, and EstimateScore between TGIF2 high and low expression groups. (D, E) Comparison of immune cell enrichment scores in high and low TGIF2 expression groups. (F) The lollipop chart showing the correlations between the relative abundances of 24 immune cells and TGIF2 expression levels. (G–N) Scatterplots demonstrating the positive correlation of TGIF2 expression with Th2 cells, macrophages, eosinophils, and neutrophils, and the negative correlation with mast cells, NK CD56bright cells, pDC cells, and TFH cells. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ns, not significant.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Expressing, Comparison

Analysis of genes coexpressed with TGIF2 in glioma. (A) Heatmap showing the 30 genes in glioma that were 15 positively and 15 negatively related to TGIF2. (B) PPI network of top 50 protein-coding genes positively and negatively correlated with TGIF2. (C) The top 10 hub genes of the PPI network in (B) . (D) The expression levels of the top 10 hub genes in normal and glioma tissues in TCGA and GTEx database. ∗∗∗p < 0.001.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Analysis of genes coexpressed with TGIF2 in glioma. (A) Heatmap showing the 30 genes in glioma that were 15 positively and 15 negatively related to TGIF2. (B) PPI network of top 50 protein-coding genes positively and negatively correlated with TGIF2. (C) The top 10 hub genes of the PPI network in (B) . (D) The expression levels of the top 10 hub genes in normal and glioma tissues in TCGA and GTEx database. ∗∗∗p < 0.001.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Expressing

Knockdown of TGIF2 inhibits glioma cell invasion, migration and EMT in vitro . (A) Bar graph demonstrating the efficiency of siRNA knockdown of TGIF2 mRNA in U251 cells by RT-qPCR. (B) Western blot assay showing that siRNA effectively knocked down TGIF2 protein, and siTGIF2 downregulated N-cadherin protein expression in U251 cells. (C) Transwell assay demonstrating changes in the number of cells invaded after knockdown of TGIF2. Scale bar, 500 μm. (D) Scratch wound-healing assays were utilized to compare the distance of cell migration between TGIF2-inhibited group and control group at 0h and 24h after scratching. Scale bar, 500 μm. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Knockdown of TGIF2 inhibits glioma cell invasion, migration and EMT in vitro . (A) Bar graph demonstrating the efficiency of siRNA knockdown of TGIF2 mRNA in U251 cells by RT-qPCR. (B) Western blot assay showing that siRNA effectively knocked down TGIF2 protein, and siTGIF2 downregulated N-cadherin protein expression in U251 cells. (C) Transwell assay demonstrating changes in the number of cells invaded after knockdown of TGIF2. Scale bar, 500 μm. (D) Scratch wound-healing assays were utilized to compare the distance of cell migration between TGIF2-inhibited group and control group at 0h and 24h after scratching. Scale bar, 500 μm. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Knockdown, Migration, In Vitro, Quantitative RT-PCR, Western Blot, Expressing, Transwell Assay, Control

Knockout of TGIF2 suppresses glioma cell invasion, migration and EMT. (A) The gRNA sequences designed targeting exon 2 of TGIF2. (B) The editing efficiency of gRNA33 and gRNA140 on TGIF2 was verified in 293T cells utilizing Sanger sequencing. (C) TGIF2-gRNA33 in the UCSC browser. (D) Western blot assay showing the knockout efficiency of TGIF2 protein. WT, Wild type; KO, Knockout. (E) Transwell assays showing changes in the number of cells invaded after knockout of TGIF2. Scale bar, 500 μm. (F) Scratch wound-healing assays were utilized to compare the distance of cell migration between TGIF2-knockout group and control group at 0h and 24h after scratching. Scale bar, 250 μm. ∗p < 0.05.

Journal: Frontiers in Immunology

Article Title: TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

doi: 10.3389/fimmu.2024.1356833

Figure Lengend Snippet: Knockout of TGIF2 suppresses glioma cell invasion, migration and EMT. (A) The gRNA sequences designed targeting exon 2 of TGIF2. (B) The editing efficiency of gRNA33 and gRNA140 on TGIF2 was verified in 293T cells utilizing Sanger sequencing. (C) TGIF2-gRNA33 in the UCSC browser. (D) Western blot assay showing the knockout efficiency of TGIF2 protein. WT, Wild type; KO, Knockout. (E) Transwell assays showing changes in the number of cells invaded after knockout of TGIF2. Scale bar, 500 μm. (F) Scratch wound-healing assays were utilized to compare the distance of cell migration between TGIF2-knockout group and control group at 0h and 24h after scratching. Scale bar, 250 μm. ∗p < 0.05.

Article Snippet: The mRNA expression data of TGIF2 in normal tissues and subcellular localization of TGIF2 protein in SH-SY5Y cell line were sourced from Human Protein Atlas (HPA) database ( http://www.proteinatlas.org/ ).

Techniques: Knock-Out, Migration, Sequencing, Western Blot, Control

( A ) A representative Kaplan–Meier analysis of overall survival of HNSCC patients ( n = 81) stratified according to DDB2 expression in tumors. Patients with higher DDB2 expression survived longer compared to patients with lower DDB2 expression, significant at alpha level of 0.05 (log rank p = 0.0404). ( B ) Loss of DDB2 expression in HNSCCs. DDB2-immunohistochemistry of human tissue microarrays (US Biomax # HN242a and HN811a). Representative images from normal tongue tissue, tongue SCCs of grades 1–3 stage I–III and cancer adjacent normal tongue tissue (NAT), normal larynx tissues and larynx SCCs grade 2 stage III and IV are shown. Scale bar for all the images, 10 μm. ( C ) The average intensity of DDB2 staining of normal tongue versus tongue SCCs showed lower staining in all SCC tissues and acute loss of staining in advanced SCCs. p < 0.0001.

Journal: Oncotarget

Article Title: DDB2 regulates Epithelial-to-Mesenchymal Transition (EMT) in Oral/Head and Neck Squamous Cell Carcinoma

doi: 10.18632/oncotarget.26168

Figure Lengend Snippet: ( A ) A representative Kaplan–Meier analysis of overall survival of HNSCC patients ( n = 81) stratified according to DDB2 expression in tumors. Patients with higher DDB2 expression survived longer compared to patients with lower DDB2 expression, significant at alpha level of 0.05 (log rank p = 0.0404). ( B ) Loss of DDB2 expression in HNSCCs. DDB2-immunohistochemistry of human tissue microarrays (US Biomax # HN242a and HN811a). Representative images from normal tongue tissue, tongue SCCs of grades 1–3 stage I–III and cancer adjacent normal tongue tissue (NAT), normal larynx tissues and larynx SCCs grade 2 stage III and IV are shown. Scale bar for all the images, 10 μm. ( C ) The average intensity of DDB2 staining of normal tongue versus tongue SCCs showed lower staining in all SCC tissues and acute loss of staining in advanced SCCs. p < 0.0001.

Article Snippet: A representative DDB2 expression data in normal tongue tissues, tongue SCCs, normal larynx and larynx SCCs from US-Biomax arrays is shown in Figure .

Techniques: Expressing, Immunohistochemistry, Staining

Mutational landscape of SMGs in HCC. (A) Significantly mutated genes in HCC. The different colors represent different mutation types. (B) Expression of SMGs in HCC and normal tissues. According to an analysis of immunohistochemical staining data from the Human Protein Atlas database, the expression of SMGs in HCC was compared with that in normal tissues.

Journal: Frontiers in Genetics

Article Title: Construction of a Comprehensive Multiomics Map of Hepatocellular Carcinoma and Screening of Possible Driver Genes

doi: 10.3389/fgene.2020.00634

Figure Lengend Snippet: Mutational landscape of SMGs in HCC. (A) Significantly mutated genes in HCC. The different colors represent different mutation types. (B) Expression of SMGs in HCC and normal tissues. According to an analysis of immunohistochemical staining data from the Human Protein Atlas database, the expression of SMGs in HCC was compared with that in normal tissues.

Article Snippet: After identifying SMGs, we obtained the expression of SMGs in HCC and normal liver tissues in Human Protein Atlas database ( https://www.proteinatlas.org/ ).

Techniques: Mutagenesis, Expressing, Immunohistochemical staining, Staining

Mutation signatures operative in HCC. (A) Single nucleotide variation classification: different colors represent different types of variation. (B) Variant classification: different colors represent different variant classifications. (C) Mutational signatures: spectrum of total SNVs and three mutational signatures in the context of the 96 base-pair substitutions. Because the dynamic range for the signatures is large, the upper limits of the y-axis used for each signature are different. (D) SMG mutation rate in three groups of HCC samples. (E) Unsupervised clustering of mutations in SMGs and focal SCNAs. (F) Differences in mutational patterns between APOBEC-enriched and non-APOBEC-enriched samples.

Journal: Frontiers in Genetics

Article Title: Construction of a Comprehensive Multiomics Map of Hepatocellular Carcinoma and Screening of Possible Driver Genes

doi: 10.3389/fgene.2020.00634

Figure Lengend Snippet: Mutation signatures operative in HCC. (A) Single nucleotide variation classification: different colors represent different types of variation. (B) Variant classification: different colors represent different variant classifications. (C) Mutational signatures: spectrum of total SNVs and three mutational signatures in the context of the 96 base-pair substitutions. Because the dynamic range for the signatures is large, the upper limits of the y-axis used for each signature are different. (D) SMG mutation rate in three groups of HCC samples. (E) Unsupervised clustering of mutations in SMGs and focal SCNAs. (F) Differences in mutational patterns between APOBEC-enriched and non-APOBEC-enriched samples.

Article Snippet: After identifying SMGs, we obtained the expression of SMGs in HCC and normal liver tissues in Human Protein Atlas database ( https://www.proteinatlas.org/ ).

Techniques: Mutagenesis, Variant Assay

(A &B) Contingency tables used to determine the likelihood of detecting a clinical (A) ADC and (B) CAR T target in the PDX human tumor N -glycoproteome against all other surface proteins in the human proteome. P-values were calculated using a Fisher’s exact test. (C) Normal tissue toxicity scoring system. (D) Distribution of full body normal tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Jiang et al., (left), Human Protein Atlas (middle) and GTEx RNA-seq data (right). (E) Distribution of normal brain tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Tushaus et al., (left), Human Protein Atlas brain IHC data (middle) and Human Protein Atlas brain RNA-seq data (right). (F) Distribution of normal heart tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Berg Luecke et al., (left) and Doll et al., (middle & right). (D-F) P-values from unpaired Mann-Whitney U tests.

Journal: bioRxiv

Article Title: Pan-cancer N -glycoproteomic atlas of patient-derived xenografts uncovers FAT2 as a therapeutic target for head and neck cancers

doi: 10.1101/2024.12.11.627962

Figure Lengend Snippet: (A &B) Contingency tables used to determine the likelihood of detecting a clinical (A) ADC and (B) CAR T target in the PDX human tumor N -glycoproteome against all other surface proteins in the human proteome. P-values were calculated using a Fisher’s exact test. (C) Normal tissue toxicity scoring system. (D) Distribution of full body normal tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Jiang et al., (left), Human Protein Atlas (middle) and GTEx RNA-seq data (right). (E) Distribution of normal brain tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Tushaus et al., (left), Human Protein Atlas brain IHC data (middle) and Human Protein Atlas brain RNA-seq data (right). (F) Distribution of normal heart tissue abundance or detection frequency of PDX target candidates (purple) vs solid tumor clinical immunotherapy targets (grey) in Berg Luecke et al., (left) and Doll et al., (middle & right). (D-F) P-values from unpaired Mann-Whitney U tests.

Article Snippet: Normal tissue IHC data were downloaded from Human Protein Atlas (v.23.0) .

Techniques: Glycoproteomics, RNA Sequencing, MANN-WHITNEY