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human tissue  (OriGene)


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    Structured Review

    OriGene human tissue
    Human Tissue, supplied by OriGene, used in various techniques. Bioz Stars score: 91/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tissuescan+prostate+cancer+tissue+array+i/TissueScan%2C+Prostate+Cancer+cDNA+Array+I/pm37566052-46-6-9
    Average 91 stars, based on 5 article reviews
    human tissue - by Bioz Stars, 2026-10
    91/100 stars

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    Related Articles

    Real-time Polymerase Chain Reaction:

    Article Title: The tyrosine receptor kinase of Axl is an essential regulator of prostate cancer proliferation and tumor growth and represents a new therapeutic target
    Article Snippet: Real-time PCR Total RNA was harvested using QIAshredder (Qiagen, Valencia, CA) and the RNeasy mini kit (Qiagen). .. Real time PCR in clinical samples was performed using the Origene TissueScan Prostate Cancer Tissue Array I and II (OriGene Technologies, Rockville MD) according to the manufacturer’s protocol. .. Primers used for real-time PCR and details are described in Supplementary Data. siRNA lentiviral vectors Mission shRNA Lentiviral Transduction Particles were obtained from Sigma Aldrich (St Louis, MO).

    Expressing:

    Article Title: DCUN1D1 Is an Essential Regulator of Prostate Cancer Proliferation and Tumour Growth That Acts through Neddylation of Cullin 1, 3, 4A and 5 and Deregulation of Wnt/Catenin Pathway
    Article Snippet: Real-time PCR: Total RNA was harvested using QIAshredder (Qiagen, Valencia, CA, USA) and the RNeasy mini kit (Qiagen) for tissue samples or cells, as recommended by the manufacturer. .. For evaluation of DCUN1D1 expression in human tissue samples, OriGene TissueScan Prostate Cancer Tissue Array I (OriGene Technologies, Rockville, MD, USA) was analysed by RT-PCR following the manufacturer’s protocol. ..

    Reverse Transcription Polymerase Chain Reaction:

    Article Title: DCUN1D1 Is an Essential Regulator of Prostate Cancer Proliferation and Tumour Growth That Acts through Neddylation of Cullin 1, 3, 4A and 5 and Deregulation of Wnt/Catenin Pathway
    Article Snippet: Real-time PCR: Total RNA was harvested using QIAshredder (Qiagen, Valencia, CA, USA) and the RNeasy mini kit (Qiagen) for tissue samples or cells, as recommended by the manufacturer. .. For evaluation of DCUN1D1 expression in human tissue samples, OriGene TissueScan Prostate Cancer Tissue Array I (OriGene Technologies, Rockville, MD, USA) was analysed by RT-PCR following the manufacturer’s protocol. ..



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    Figure 1 Overview of the lncRNA GHSROS and its expression in cancer. (A) The GHSR and GHSROS gene loci. GHSR exons (black), GHSROS exon (red), repetitive elements (orange), introns (lines). (B) GH- SROS expression in 19 cancers <t>(TissueScan</t> Cancer Survey Tissue <t>qPCR</t> panel). N (black) denotes nor- mal tissue; T tumor (red). For each cancer, data are expressed as mean fold change using the compara- tive 2−11Ct method against a non-malignant control tissue. Normalized to β-actin (ACTB). (C) Relative gene expression of GHSROS in OriGene cDNA panels of tissues from normal prostate (n = 24; blue), pri- mary prostate cancer (n = 88; red), and other prostatic diseases (n = 31; orange). Determined by qRT- PCR, normalized to ribosomal protein L32 (RPL32), and represented as standardized expression values (Z-scores). (D) GHSROS expression in an Andalusian Biobank prostate tissue cohort. Absolute expres- sion levels were determined by qRT-PCR and adjusted by a normalization factor calculated from the ex- pression levels of three housekeeping genes (HPRT, ACTB, and GAPDH). NP denotes non-malignant prostate. *P ≤0.05, Mann–Whitney-Wilcoxon test. (E) Expression of GHSROS in immortalized, cul- tured cell lines and patient-derived xenograft (PDX) lines. Mean ± s.e.m. (n = 3). *P ≤0.05, **P ≤0.01, *** P ≤0.001, Student’s t-test. Normalized as in (b) to the RWPE-1 non-malignant cell line. Androgen- independent lines are labeled in orange.
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    Figure 1 Overview of the lncRNA GHSROS and its expression in cancer. (A) The GHSR and GHSROS gene loci. GHSR exons (black), GHSROS exon (red), repetitive elements (orange), introns (lines). (B) GH- SROS expression in 19 cancers <t>(TissueScan</t> Cancer Survey Tissue <t>qPCR</t> panel). N (black) denotes nor- mal tissue; T tumor (red). For each cancer, data are expressed as mean fold change using the compara- tive 2−11Ct method against a non-malignant control tissue. Normalized to β-actin (ACTB). (C) Relative gene expression of GHSROS in OriGene cDNA panels of tissues from normal prostate (n = 24; blue), pri- mary prostate cancer (n = 88; red), and other prostatic diseases (n = 31; orange). Determined by qRT- PCR, normalized to ribosomal protein L32 (RPL32), and represented as standardized expression values (Z-scores). (D) GHSROS expression in an Andalusian Biobank prostate tissue cohort. Absolute expres- sion levels were determined by qRT-PCR and adjusted by a normalization factor calculated from the ex- pression levels of three housekeeping genes (HPRT, ACTB, and GAPDH). NP denotes non-malignant prostate. *P ≤0.05, Mann–Whitney-Wilcoxon test. (E) Expression of GHSROS in immortalized, cul- tured cell lines and patient-derived xenograft (PDX) lines. Mean ± s.e.m. (n = 3). *P ≤0.05, **P ≤0.01, *** P ≤0.001, Student’s t-test. Normalized as in (b) to the RWPE-1 non-malignant cell line. Androgen- independent lines are labeled in orange.
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    OriGene cap qpcr tissue arrays
    (A) Twist1 and Hoxa9 gene expression by <t>qPCR</t> in E15.5-E18.5 UGS and P0, P5 <t>developing</t> <t>prostate</t> (n=3-6 embryos-pups/time point/gene, Pearson correlation coefficient, R2= 0.82). Normalized to expression level at P35. (B) TWIST1 and HOXA9 IHC on serial sections of E17.5 UGS from wild-type mice in cells at the urogenital mesenchyme (UGM)-urogenital epithelium (UGE) interface. UGMi; section of the UGM closest to the UGE interface, UGMe; section of the UGM toward the edge. Graphs represent percentage positive cells (n=4 embryos). (C) TWIST1 and HOXA9 IHC on adjacent serial sections of prostate tissue from probasin (PB)-Cre; Apcflox/flox mice with prostate neoplasia (n=2). Arrows highlight TWIST and HOXA9 co-expression in the same cell-types.
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    Image Search Results


    Figure 1 Overview of the lncRNA GHSROS and its expression in cancer. (A) The GHSR and GHSROS gene loci. GHSR exons (black), GHSROS exon (red), repetitive elements (orange), introns (lines). (B) GH- SROS expression in 19 cancers (TissueScan Cancer Survey Tissue qPCR panel). N (black) denotes nor- mal tissue; T tumor (red). For each cancer, data are expressed as mean fold change using the compara- tive 2−11Ct method against a non-malignant control tissue. Normalized to β-actin (ACTB). (C) Relative gene expression of GHSROS in OriGene cDNA panels of tissues from normal prostate (n = 24; blue), pri- mary prostate cancer (n = 88; red), and other prostatic diseases (n = 31; orange). Determined by qRT- PCR, normalized to ribosomal protein L32 (RPL32), and represented as standardized expression values (Z-scores). (D) GHSROS expression in an Andalusian Biobank prostate tissue cohort. Absolute expres- sion levels were determined by qRT-PCR and adjusted by a normalization factor calculated from the ex- pression levels of three housekeeping genes (HPRT, ACTB, and GAPDH). NP denotes non-malignant prostate. *P ≤0.05, Mann–Whitney-Wilcoxon test. (E) Expression of GHSROS in immortalized, cul- tured cell lines and patient-derived xenograft (PDX) lines. Mean ± s.e.m. (n = 3). *P ≤0.05, **P ≤0.01, *** P ≤0.001, Student’s t-test. Normalized as in (b) to the RWPE-1 non-malignant cell line. Androgen- independent lines are labeled in orange.

    Journal: PeerJ

    Article Title: The long non-coding RNA GHSROS reprograms prostate cancer cell lines toward a more aggressive phenotype.

    doi: 10.7717/peerj.10280

    Figure Lengend Snippet: Figure 1 Overview of the lncRNA GHSROS and its expression in cancer. (A) The GHSR and GHSROS gene loci. GHSR exons (black), GHSROS exon (red), repetitive elements (orange), introns (lines). (B) GH- SROS expression in 19 cancers (TissueScan Cancer Survey Tissue qPCR panel). N (black) denotes nor- mal tissue; T tumor (red). For each cancer, data are expressed as mean fold change using the compara- tive 2−11Ct method against a non-malignant control tissue. Normalized to β-actin (ACTB). (C) Relative gene expression of GHSROS in OriGene cDNA panels of tissues from normal prostate (n = 24; blue), pri- mary prostate cancer (n = 88; red), and other prostatic diseases (n = 31; orange). Determined by qRT- PCR, normalized to ribosomal protein L32 (RPL32), and represented as standardized expression values (Z-scores). (D) GHSROS expression in an Andalusian Biobank prostate tissue cohort. Absolute expres- sion levels were determined by qRT-PCR and adjusted by a normalization factor calculated from the ex- pression levels of three housekeeping genes (HPRT, ACTB, and GAPDH). NP denotes non-malignant prostate. *P ≤0.05, Mann–Whitney-Wilcoxon test. (E) Expression of GHSROS in immortalized, cul- tured cell lines and patient-derived xenograft (PDX) lines. Mean ± s.e.m. (n = 3). *P ≤0.05, **P ≤0.01, *** P ≤0.001, Student’s t-test. Normalized as in (b) to the RWPE-1 non-malignant cell line. Androgen- independent lines are labeled in orange.

    Article Snippet: To further investigate the expression of GHSROS in prostate cancer TissueScan Prostate Cancer Tissue qPCR panels (HPRT101, HPRT102, and HPRT103) were obtained from OriGene.

    Techniques: Expressing, Control, Gene Expression, Quantitative RT-PCR, MANN-WHITNEY, Derivative Assay, Labeling

    (A) Twist1 and Hoxa9 gene expression by qPCR in E15.5-E18.5 UGS and P0, P5 developing prostate (n=3-6 embryos-pups/time point/gene, Pearson correlation coefficient, R2= 0.82). Normalized to expression level at P35. (B) TWIST1 and HOXA9 IHC on serial sections of E17.5 UGS from wild-type mice in cells at the urogenital mesenchyme (UGM)-urogenital epithelium (UGE) interface. UGMi; section of the UGM closest to the UGE interface, UGMe; section of the UGM toward the edge. Graphs represent percentage positive cells (n=4 embryos). (C) TWIST1 and HOXA9 IHC on adjacent serial sections of prostate tissue from probasin (PB)-Cre; Apcflox/flox mice with prostate neoplasia (n=2). Arrows highlight TWIST and HOXA9 co-expression in the same cell-types.

    Journal: Cancer research

    Article Title: TWIST1-WDR5- Hottip regulates Hoxa9 chromatin to facilitate prostate cancer metastasis

    doi: 10.1158/0008-5472.CAN-16-2797

    Figure Lengend Snippet: (A) Twist1 and Hoxa9 gene expression by qPCR in E15.5-E18.5 UGS and P0, P5 developing prostate (n=3-6 embryos-pups/time point/gene, Pearson correlation coefficient, R2= 0.82). Normalized to expression level at P35. (B) TWIST1 and HOXA9 IHC on serial sections of E17.5 UGS from wild-type mice in cells at the urogenital mesenchyme (UGM)-urogenital epithelium (UGE) interface. UGMi; section of the UGM closest to the UGE interface, UGMe; section of the UGM toward the edge. Graphs represent percentage positive cells (n=4 embryos). (C) TWIST1 and HOXA9 IHC on adjacent serial sections of prostate tissue from probasin (PB)-Cre; Apcflox/flox mice with prostate neoplasia (n=2). Arrows highlight TWIST and HOXA9 co-expression in the same cell-types.

    Article Snippet: Human normal prostate and CaP qPCR tissue arrays were purchased from OriGene.

    Techniques: Gene Expression, Expressing

    (A) Wdr5 shRNA knockdown in Myc-CaP-TWIST1 cells reduced Hoxa9 expression as shown by qPCR. (B) Myc-CaP-TWIST1 cells with stable knockdown of Wdr5 showed decreased migration and (C) invasion through Matrigel compared to scrambled shRNA control. (D) WDR5 knockout by TALEN in PC3-TWIST1 cells decreased HOXA9 expression. (E) PC3-TWIST1 WDR5 knockout cells had decreased cell migration and (F) invasion through Matrigel cells compared to scrambled shRNA control. (G) Knockdown of Hottip/HOTTIP by siRNA in Myc-CaP-TWIST1 or (J) PC3-TWIST1 cells, respectively, led to decreased Hoxa9/HOXA9 mRNA. (H) Hottip or (K) HOTTIP knockdown led to decreased cell migration and (I) and (L) invasion through Matrigel in Myc-CaP-TWIST1 and PC3-TWIST1 cells, respectively, compared to scrambled control. All were n≥3, Mann-Whitney t-test: *, p< 0.05; **, p< 0.01; ***, p< 0.001, +/-SEM.

    Journal: Cancer research

    Article Title: TWIST1-WDR5- Hottip regulates Hoxa9 chromatin to facilitate prostate cancer metastasis

    doi: 10.1158/0008-5472.CAN-16-2797

    Figure Lengend Snippet: (A) Wdr5 shRNA knockdown in Myc-CaP-TWIST1 cells reduced Hoxa9 expression as shown by qPCR. (B) Myc-CaP-TWIST1 cells with stable knockdown of Wdr5 showed decreased migration and (C) invasion through Matrigel compared to scrambled shRNA control. (D) WDR5 knockout by TALEN in PC3-TWIST1 cells decreased HOXA9 expression. (E) PC3-TWIST1 WDR5 knockout cells had decreased cell migration and (F) invasion through Matrigel cells compared to scrambled shRNA control. (G) Knockdown of Hottip/HOTTIP by siRNA in Myc-CaP-TWIST1 or (J) PC3-TWIST1 cells, respectively, led to decreased Hoxa9/HOXA9 mRNA. (H) Hottip or (K) HOTTIP knockdown led to decreased cell migration and (I) and (L) invasion through Matrigel in Myc-CaP-TWIST1 and PC3-TWIST1 cells, respectively, compared to scrambled control. All were n≥3, Mann-Whitney t-test: *, p< 0.05; **, p< 0.01; ***, p< 0.001, +/-SEM.

    Article Snippet: Human normal prostate and CaP qPCR tissue arrays were purchased from OriGene.

    Techniques: shRNA, Knockdown, Expressing, Migration, Control, Knock-Out, MANN-WHITNEY