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human hepatocellular carcinoma hcc cell line huh7  (Procell Inc)

 
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    Structured Review

    Procell Inc human hepatocellular carcinoma hcc cell line huh7
    Network pharmacology analysis of ECH treatment for <t>HCC.</t> ( A ) The chemical structure of ECH. ( B ) Intersection of ECH and HCC targets. ( C ) Intersection of ECH, HCC, and ferroptosis targets. ( D ) PPI network analysis of the intersection of ECH, HCC, and ferroptosis targets, with the inner circle showing the top ten core targets for ECH-mediated ferroptosis in HCC. ( E ) The top ten core targets for ECH-mediated regulation of HCC ferroptosis, with TP53 as the primary core target. Abbreviations: ECH: echinacoside. HCC: <t>hepatocellular</t> carcinoma. PPI: protein–protein interaction.
    Human Hepatocellular Carcinoma Hcc Cell Line Huh7, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+hepatocellular+carcinoma+hcc+cell+line+huh7/7+huh/pmc12787297-192-13-23
    Average 86 stars, based on 1 article reviews
    human hepatocellular carcinoma hcc cell line huh7 - by Bioz Stars, 2026-08
    86/100 stars

    Images

    1) Product Images from "Echinacoside as a Novel Ferroptosis Inducer in Hepatocellular Carcinoma: Mechanistic Insights from TP53/SLC7A11/GPX4 Pathway Modulation"

    Article Title: Echinacoside as a Novel Ferroptosis Inducer in Hepatocellular Carcinoma: Mechanistic Insights from TP53/SLC7A11/GPX4 Pathway Modulation

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms27010411

    Network pharmacology analysis of ECH treatment for HCC. ( A ) The chemical structure of ECH. ( B ) Intersection of ECH and HCC targets. ( C ) Intersection of ECH, HCC, and ferroptosis targets. ( D ) PPI network analysis of the intersection of ECH, HCC, and ferroptosis targets, with the inner circle showing the top ten core targets for ECH-mediated ferroptosis in HCC. ( E ) The top ten core targets for ECH-mediated regulation of HCC ferroptosis, with TP53 as the primary core target. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. PPI: protein–protein interaction.
    Figure Legend Snippet: Network pharmacology analysis of ECH treatment for HCC. ( A ) The chemical structure of ECH. ( B ) Intersection of ECH and HCC targets. ( C ) Intersection of ECH, HCC, and ferroptosis targets. ( D ) PPI network analysis of the intersection of ECH, HCC, and ferroptosis targets, with the inner circle showing the top ten core targets for ECH-mediated ferroptosis in HCC. ( E ) The top ten core targets for ECH-mediated regulation of HCC ferroptosis, with TP53 as the primary core target. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. PPI: protein–protein interaction.

    Techniques Used:

    Functional enrichment analyses of ECH against HCC. ( A ) Lollipop chart of KEGG analysis for ECH treatment of HCC. ( B ) Lollipop chart showing the MF section of the GO analysis for ECH treatment of HCC. Abbreviations: KEGG: Kyoto Encyclopedia of Genes and Genomes. ECH: echinacoside. HCC: hepatocellular carcinoma. MF: molecular function. GO: Gene Ontology.
    Figure Legend Snippet: Functional enrichment analyses of ECH against HCC. ( A ) Lollipop chart of KEGG analysis for ECH treatment of HCC. ( B ) Lollipop chart showing the MF section of the GO analysis for ECH treatment of HCC. Abbreviations: KEGG: Kyoto Encyclopedia of Genes and Genomes. ECH: echinacoside. HCC: hepatocellular carcinoma. MF: molecular function. GO: Gene Ontology.

    Techniques Used: Functional Assay

    The results of HCC cell growth inhibited by ECH. ( A ) HepG2 cells were treated with different concentrations of ECH for 24 h. ( B ) Huh7 cells were treated with different concentrations of ECH for 24 h. ( C ) LO2 cells were treated with different concentrations of ECH for 24 h. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. IC 50 : half-maximal inhibitory concentration.
    Figure Legend Snippet: The results of HCC cell growth inhibited by ECH. ( A ) HepG2 cells were treated with different concentrations of ECH for 24 h. ( B ) Huh7 cells were treated with different concentrations of ECH for 24 h. ( C ) LO2 cells were treated with different concentrations of ECH for 24 h. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. IC 50 : half-maximal inhibitory concentration.

    Techniques Used: Concentration Assay

    Ferroptosis in HCC cells induced by ECH. ( A ) LPO levels in HepG2 and Huh7 cells treated with erastin (10 μmol/L), Fer-1 (2 μmol/L), and ECH for 24 h were detected and quantified using fluorescence inverted microscopy. ( B ) Fe 2+ levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. ( C ) GSH levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. ( D ) MDA levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. The plus sign (+) indicates drug intervention, and the minus sign (−) indicates absence of the drug. Data were represented as mean ± SD ( n = 3); ns = no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 versus control group. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. Fer-1: ferrostatin-1. GSH: glutathione. MDA: malondialdehyde.
    Figure Legend Snippet: Ferroptosis in HCC cells induced by ECH. ( A ) LPO levels in HepG2 and Huh7 cells treated with erastin (10 μmol/L), Fer-1 (2 μmol/L), and ECH for 24 h were detected and quantified using fluorescence inverted microscopy. ( B ) Fe 2+ levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. ( C ) GSH levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. ( D ) MDA levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. The plus sign (+) indicates drug intervention, and the minus sign (−) indicates absence of the drug. Data were represented as mean ± SD ( n = 3); ns = no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 versus control group. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. Fer-1: ferrostatin-1. GSH: glutathione. MDA: malondialdehyde.

    Techniques Used: Fluorescence, Inverted Microscopy, Control

    Ferroptosis induced by ECH in HCC cells via the TP53/SLC7A11/GPX4 signaling pathway. ( A ) Kaplan-Meier univariate survival analysis of TP53 expression in HCC versus normal tissues. ( B ) The TP53, SLC7A11, and GPX4 mRNA levels in HepG2 and Huh7 cells following a 24 h treatment with various concentrations of ECH and Fer-1 (2 μmol/L). ( C ) The TP53, SLC7A11, and GPX4 protein expression levels in HepG2 cells after 24 h treatment with different concentrations of ECH and Fer-1 (2 μmol/L). ( D ) The protein expression levels of TP53, SLC7A11, and GPX4 in Huh7 cells after treatment with different concentrations of ECH and Fer-1 (2 μmol/L) for 24 h. Data are represented as mean ± SD ( n = 3); ns = no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 vs. control group. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. TP53: tumor protein 53. Fer-1: ferrostatin-1. SLC7A11: solute carrier family 7 member 11. GPX4: glutathione peroxidase 4.
    Figure Legend Snippet: Ferroptosis induced by ECH in HCC cells via the TP53/SLC7A11/GPX4 signaling pathway. ( A ) Kaplan-Meier univariate survival analysis of TP53 expression in HCC versus normal tissues. ( B ) The TP53, SLC7A11, and GPX4 mRNA levels in HepG2 and Huh7 cells following a 24 h treatment with various concentrations of ECH and Fer-1 (2 μmol/L). ( C ) The TP53, SLC7A11, and GPX4 protein expression levels in HepG2 cells after 24 h treatment with different concentrations of ECH and Fer-1 (2 μmol/L). ( D ) The protein expression levels of TP53, SLC7A11, and GPX4 in Huh7 cells after treatment with different concentrations of ECH and Fer-1 (2 μmol/L) for 24 h. Data are represented as mean ± SD ( n = 3); ns = no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 vs. control group. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. TP53: tumor protein 53. Fer-1: ferrostatin-1. SLC7A11: solute carrier family 7 member 11. GPX4: glutathione peroxidase 4.

    Techniques Used: Expressing, Control



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    Procell Inc human hepatocellular carcinoma hcc cell line huh7
    Network pharmacology analysis of ECH treatment for <t>HCC.</t> ( A ) The chemical structure of ECH. ( B ) Intersection of ECH and HCC targets. ( C ) Intersection of ECH, HCC, and ferroptosis targets. ( D ) PPI network analysis of the intersection of ECH, HCC, and ferroptosis targets, with the inner circle showing the top ten core targets for ECH-mediated ferroptosis in HCC. ( E ) The top ten core targets for ECH-mediated regulation of HCC ferroptosis, with TP53 as the primary core target. Abbreviations: ECH: echinacoside. HCC: <t>hepatocellular</t> carcinoma. PPI: protein–protein interaction.
    Human Hepatocellular Carcinoma Hcc Cell Line Huh7, supplied by Procell Inc, 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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    JCRB Cell Bank human hepatocellular carcinoma (hcc) cell line huh7 jcrb0403
    Radioiodide biodistribution in vivo after MSC-mediated NIS gene transfer. In vivo, using the <t>hepatocellular</t> carcinoma <t>(HuH7)</t> xenograft mouse model, HSP70B-NIS-MSCs were injected into the tail vein of mice, followed by hyperthermia, or as controls normothermia at 37 °C, 3 days later. 0 - 72 h after promoter activation by thermo-stimulation, 18.5 MBq 123 I were injected and serial gamma camera imaging started ( A ). Images of gamma camera imaging taken 2 h after radioiodide of animals with 0 h ( B ; n = 7), 6 h ( n = 5), 12 h ( C ; n = 7), 18 h ( n = 4), 24 h ( D ; n = 6), 36 h ( n = 4), 48 h ( n = 5) and 72 h ( E ; n = 4) between promoter activation by hyperthermia and radioiodine injection and control animals, treated at 37 °C ( F ; n = 5) (one representative image for each treatment group). Quantification of serial 123 I-scintigraphy ( G ) representing the efflux of the injected 123 I and comparison of the tumoral 123 I accumulation 1 h post injection ( H ) (the blue line represents the controls at 37 °C). Results are expressed as mean ± SEM; two-way ANOVA with post-hoc Tukey test * p < 0.05.
    Human Hepatocellular Carcinoma (Hcc) Cell Line Huh7 Jcrb0403, supplied by JCRB Cell Bank, 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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    Network pharmacology analysis of ECH treatment for HCC. ( A ) The chemical structure of ECH. ( B ) Intersection of ECH and HCC targets. ( C ) Intersection of ECH, HCC, and ferroptosis targets. ( D ) PPI network analysis of the intersection of ECH, HCC, and ferroptosis targets, with the inner circle showing the top ten core targets for ECH-mediated ferroptosis in HCC. ( E ) The top ten core targets for ECH-mediated regulation of HCC ferroptosis, with TP53 as the primary core target. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. PPI: protein–protein interaction.

    Journal: International Journal of Molecular Sciences

    Article Title: Echinacoside as a Novel Ferroptosis Inducer in Hepatocellular Carcinoma: Mechanistic Insights from TP53/SLC7A11/GPX4 Pathway Modulation

    doi: 10.3390/ijms27010411

    Figure Lengend Snippet: Network pharmacology analysis of ECH treatment for HCC. ( A ) The chemical structure of ECH. ( B ) Intersection of ECH and HCC targets. ( C ) Intersection of ECH, HCC, and ferroptosis targets. ( D ) PPI network analysis of the intersection of ECH, HCC, and ferroptosis targets, with the inner circle showing the top ten core targets for ECH-mediated ferroptosis in HCC. ( E ) The top ten core targets for ECH-mediated regulation of HCC ferroptosis, with TP53 as the primary core target. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. PPI: protein–protein interaction.

    Article Snippet: The human normal hepatocytes cell line LO2, human hepatoblastoma cell line HepG2, and human hepatocellular carcinoma (HCC) cell line HuH7 were obtained from Procell (Wuhan, China).

    Techniques:

    Functional enrichment analyses of ECH against HCC. ( A ) Lollipop chart of KEGG analysis for ECH treatment of HCC. ( B ) Lollipop chart showing the MF section of the GO analysis for ECH treatment of HCC. Abbreviations: KEGG: Kyoto Encyclopedia of Genes and Genomes. ECH: echinacoside. HCC: hepatocellular carcinoma. MF: molecular function. GO: Gene Ontology.

    Journal: International Journal of Molecular Sciences

    Article Title: Echinacoside as a Novel Ferroptosis Inducer in Hepatocellular Carcinoma: Mechanistic Insights from TP53/SLC7A11/GPX4 Pathway Modulation

    doi: 10.3390/ijms27010411

    Figure Lengend Snippet: Functional enrichment analyses of ECH against HCC. ( A ) Lollipop chart of KEGG analysis for ECH treatment of HCC. ( B ) Lollipop chart showing the MF section of the GO analysis for ECH treatment of HCC. Abbreviations: KEGG: Kyoto Encyclopedia of Genes and Genomes. ECH: echinacoside. HCC: hepatocellular carcinoma. MF: molecular function. GO: Gene Ontology.

    Article Snippet: The human normal hepatocytes cell line LO2, human hepatoblastoma cell line HepG2, and human hepatocellular carcinoma (HCC) cell line HuH7 were obtained from Procell (Wuhan, China).

    Techniques: Functional Assay

    The results of HCC cell growth inhibited by ECH. ( A ) HepG2 cells were treated with different concentrations of ECH for 24 h. ( B ) Huh7 cells were treated with different concentrations of ECH for 24 h. ( C ) LO2 cells were treated with different concentrations of ECH for 24 h. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. IC 50 : half-maximal inhibitory concentration.

    Journal: International Journal of Molecular Sciences

    Article Title: Echinacoside as a Novel Ferroptosis Inducer in Hepatocellular Carcinoma: Mechanistic Insights from TP53/SLC7A11/GPX4 Pathway Modulation

    doi: 10.3390/ijms27010411

    Figure Lengend Snippet: The results of HCC cell growth inhibited by ECH. ( A ) HepG2 cells were treated with different concentrations of ECH for 24 h. ( B ) Huh7 cells were treated with different concentrations of ECH for 24 h. ( C ) LO2 cells were treated with different concentrations of ECH for 24 h. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. IC 50 : half-maximal inhibitory concentration.

    Article Snippet: The human normal hepatocytes cell line LO2, human hepatoblastoma cell line HepG2, and human hepatocellular carcinoma (HCC) cell line HuH7 were obtained from Procell (Wuhan, China).

    Techniques: Concentration Assay

    Ferroptosis in HCC cells induced by ECH. ( A ) LPO levels in HepG2 and Huh7 cells treated with erastin (10 μmol/L), Fer-1 (2 μmol/L), and ECH for 24 h were detected and quantified using fluorescence inverted microscopy. ( B ) Fe 2+ levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. ( C ) GSH levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. ( D ) MDA levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. The plus sign (+) indicates drug intervention, and the minus sign (−) indicates absence of the drug. Data were represented as mean ± SD ( n = 3); ns = no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 versus control group. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. Fer-1: ferrostatin-1. GSH: glutathione. MDA: malondialdehyde.

    Journal: International Journal of Molecular Sciences

    Article Title: Echinacoside as a Novel Ferroptosis Inducer in Hepatocellular Carcinoma: Mechanistic Insights from TP53/SLC7A11/GPX4 Pathway Modulation

    doi: 10.3390/ijms27010411

    Figure Lengend Snippet: Ferroptosis in HCC cells induced by ECH. ( A ) LPO levels in HepG2 and Huh7 cells treated with erastin (10 μmol/L), Fer-1 (2 μmol/L), and ECH for 24 h were detected and quantified using fluorescence inverted microscopy. ( B ) Fe 2+ levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. ( C ) GSH levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. ( D ) MDA levels after treated with ECH (300 µmol/L) and Fer-1 (2 µmol/L) for 24 h in HepG2 and Huh7 cells. The plus sign (+) indicates drug intervention, and the minus sign (−) indicates absence of the drug. Data were represented as mean ± SD ( n = 3); ns = no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 versus control group. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. Fer-1: ferrostatin-1. GSH: glutathione. MDA: malondialdehyde.

    Article Snippet: The human normal hepatocytes cell line LO2, human hepatoblastoma cell line HepG2, and human hepatocellular carcinoma (HCC) cell line HuH7 were obtained from Procell (Wuhan, China).

    Techniques: Fluorescence, Inverted Microscopy, Control

    Ferroptosis induced by ECH in HCC cells via the TP53/SLC7A11/GPX4 signaling pathway. ( A ) Kaplan-Meier univariate survival analysis of TP53 expression in HCC versus normal tissues. ( B ) The TP53, SLC7A11, and GPX4 mRNA levels in HepG2 and Huh7 cells following a 24 h treatment with various concentrations of ECH and Fer-1 (2 μmol/L). ( C ) The TP53, SLC7A11, and GPX4 protein expression levels in HepG2 cells after 24 h treatment with different concentrations of ECH and Fer-1 (2 μmol/L). ( D ) The protein expression levels of TP53, SLC7A11, and GPX4 in Huh7 cells after treatment with different concentrations of ECH and Fer-1 (2 μmol/L) for 24 h. Data are represented as mean ± SD ( n = 3); ns = no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 vs. control group. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. TP53: tumor protein 53. Fer-1: ferrostatin-1. SLC7A11: solute carrier family 7 member 11. GPX4: glutathione peroxidase 4.

    Journal: International Journal of Molecular Sciences

    Article Title: Echinacoside as a Novel Ferroptosis Inducer in Hepatocellular Carcinoma: Mechanistic Insights from TP53/SLC7A11/GPX4 Pathway Modulation

    doi: 10.3390/ijms27010411

    Figure Lengend Snippet: Ferroptosis induced by ECH in HCC cells via the TP53/SLC7A11/GPX4 signaling pathway. ( A ) Kaplan-Meier univariate survival analysis of TP53 expression in HCC versus normal tissues. ( B ) The TP53, SLC7A11, and GPX4 mRNA levels in HepG2 and Huh7 cells following a 24 h treatment with various concentrations of ECH and Fer-1 (2 μmol/L). ( C ) The TP53, SLC7A11, and GPX4 protein expression levels in HepG2 cells after 24 h treatment with different concentrations of ECH and Fer-1 (2 μmol/L). ( D ) The protein expression levels of TP53, SLC7A11, and GPX4 in Huh7 cells after treatment with different concentrations of ECH and Fer-1 (2 μmol/L) for 24 h. Data are represented as mean ± SD ( n = 3); ns = no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 vs. control group. Abbreviations: ECH: echinacoside. HCC: hepatocellular carcinoma. TP53: tumor protein 53. Fer-1: ferrostatin-1. SLC7A11: solute carrier family 7 member 11. GPX4: glutathione peroxidase 4.

    Article Snippet: The human normal hepatocytes cell line LO2, human hepatoblastoma cell line HepG2, and human hepatocellular carcinoma (HCC) cell line HuH7 were obtained from Procell (Wuhan, China).

    Techniques: Expressing, Control

    Radioiodide biodistribution in vivo after MSC-mediated NIS gene transfer. In vivo, using the hepatocellular carcinoma (HuH7) xenograft mouse model, HSP70B-NIS-MSCs were injected into the tail vein of mice, followed by hyperthermia, or as controls normothermia at 37 °C, 3 days later. 0 - 72 h after promoter activation by thermo-stimulation, 18.5 MBq 123 I were injected and serial gamma camera imaging started ( A ). Images of gamma camera imaging taken 2 h after radioiodide of animals with 0 h ( B ; n = 7), 6 h ( n = 5), 12 h ( C ; n = 7), 18 h ( n = 4), 24 h ( D ; n = 6), 36 h ( n = 4), 48 h ( n = 5) and 72 h ( E ; n = 4) between promoter activation by hyperthermia and radioiodine injection and control animals, treated at 37 °C ( F ; n = 5) (one representative image for each treatment group). Quantification of serial 123 I-scintigraphy ( G ) representing the efflux of the injected 123 I and comparison of the tumoral 123 I accumulation 1 h post injection ( H ) (the blue line represents the controls at 37 °C). Results are expressed as mean ± SEM; two-way ANOVA with post-hoc Tukey test * p < 0.05.

    Journal: Theranostics

    Article Title: Effective control of tumor growth through spatial and temporal control of theranostic sodium iodide symporter ( NIS ) gene expression using a heat-inducible gene promoter in engineered mesenchymal stem cells

    doi: 10.7150/thno.41489

    Figure Lengend Snippet: Radioiodide biodistribution in vivo after MSC-mediated NIS gene transfer. In vivo, using the hepatocellular carcinoma (HuH7) xenograft mouse model, HSP70B-NIS-MSCs were injected into the tail vein of mice, followed by hyperthermia, or as controls normothermia at 37 °C, 3 days later. 0 - 72 h after promoter activation by thermo-stimulation, 18.5 MBq 123 I were injected and serial gamma camera imaging started ( A ). Images of gamma camera imaging taken 2 h after radioiodide of animals with 0 h ( B ; n = 7), 6 h ( n = 5), 12 h ( C ; n = 7), 18 h ( n = 4), 24 h ( D ; n = 6), 36 h ( n = 4), 48 h ( n = 5) and 72 h ( E ; n = 4) between promoter activation by hyperthermia and radioiodine injection and control animals, treated at 37 °C ( F ; n = 5) (one representative image for each treatment group). Quantification of serial 123 I-scintigraphy ( G ) representing the efflux of the injected 123 I and comparison of the tumoral 123 I accumulation 1 h post injection ( H ) (the blue line represents the controls at 37 °C). Results are expressed as mean ± SEM; two-way ANOVA with post-hoc Tukey test * p < 0.05.

    Article Snippet: The human hepatocellular carcinoma (HCC) cell line HuH7 (JCRB0403; Japanese Collection of Research Bioresources Cell Bank, Osaka, Japan) was grown in Dulbecco's Modified Eagle Medium (1 g/l glucose; Sigma Aldrich, St. Louis, Missouri, USA) supplemented with 10% (v/v) fetal bovine serum (FBS; FBS Superior, Biochrom GmbH, Berlin, Germany) and 100 U/ml penicillin and 100 μg/ml streptomycin (P/S; Sigma-Aldrich).

    Techniques: In Vivo, Injection, Activation Assay, Imaging, Control, Comparison

    Ex vivo analysis of NIS expression. NIS-specific immunohistochemistry (red) was performed on paraffin-embedded HuH7 tumor sections. Tumors of mice of 37 °C controls ( A ) compared to mice which were heat-treated with a 12 h latency between promoter activation and 123 I administration ( B ). Control organs (liver, lung, spleen, and kidney) of mice receiving 37 °C ( C ) or 41 °C ( D ) treatment. One representative image is shown each at 2x - 73x magnification for tumor sections and 20x for control organs. mRNA was isolated from frozen tumors sections of heat treated mice (groups in which 0, 12, 18, and 36 h were in between promoter activation and start of 123 I-scintigraphy) and controls (37 °C) at the end of the serial gamma camera imaging and analyzed for NIS ( E ), endogenous HSPA1A ( F ) and HSPA7 ( G ) by RT-PCR ( n = 4; one-way ANOVA; * p < 0.05, *** p < 0.001).

    Journal: Theranostics

    Article Title: Effective control of tumor growth through spatial and temporal control of theranostic sodium iodide symporter ( NIS ) gene expression using a heat-inducible gene promoter in engineered mesenchymal stem cells

    doi: 10.7150/thno.41489

    Figure Lengend Snippet: Ex vivo analysis of NIS expression. NIS-specific immunohistochemistry (red) was performed on paraffin-embedded HuH7 tumor sections. Tumors of mice of 37 °C controls ( A ) compared to mice which were heat-treated with a 12 h latency between promoter activation and 123 I administration ( B ). Control organs (liver, lung, spleen, and kidney) of mice receiving 37 °C ( C ) or 41 °C ( D ) treatment. One representative image is shown each at 2x - 73x magnification for tumor sections and 20x for control organs. mRNA was isolated from frozen tumors sections of heat treated mice (groups in which 0, 12, 18, and 36 h were in between promoter activation and start of 123 I-scintigraphy) and controls (37 °C) at the end of the serial gamma camera imaging and analyzed for NIS ( E ), endogenous HSPA1A ( F ) and HSPA7 ( G ) by RT-PCR ( n = 4; one-way ANOVA; * p < 0.05, *** p < 0.001).

    Article Snippet: The human hepatocellular carcinoma (HCC) cell line HuH7 (JCRB0403; Japanese Collection of Research Bioresources Cell Bank, Osaka, Japan) was grown in Dulbecco's Modified Eagle Medium (1 g/l glucose; Sigma Aldrich, St. Louis, Missouri, USA) supplemented with 10% (v/v) fetal bovine serum (FBS; FBS Superior, Biochrom GmbH, Berlin, Germany) and 100 U/ml penicillin and 100 μg/ml streptomycin (P/S; Sigma-Aldrich).

    Techniques: Ex Vivo, Expressing, Immunohistochemistry, Activation Assay, Control, Isolation, Imaging, Reverse Transcription Polymerase Chain Reaction

    Heat-induced MSC-mediated NIS gene therapy in vivo. Three days after systemic injections of HSP70B-NIS-MSCs (black arrows), hyperthermia (red arrows) was administered to mice harboring HuH7 xenograft tumors. 12 to 18 h later, 55.5 MBq of therapeutic 131 I (green arrows) was applied. This treatment cycle was repeated for a total of three times ( A ). Tumor growth ( B ) and overall survival ( C ) were evaluated for the treatment with HSP70B-NIS-MSCs, hyperthermia and 131 I (HSP-NIS-MSCs + 41 °C + 131 I; n = 9), compared to control groups, receiving hyperthermia and saline (NaCl + 41 °C + NaCl; n = 10) and to normothermic groups (HSP70B-NIS-MSCs + 37 °C + 131 I; n = 9 and NaCl + 37 °C + NaCl; n = 10). Results are expressed as mean ± SEM (one-way ANOVA for tumor growth and log-rank test for Kaplan-Meier survival plots; * p < 0.05; ** p < 0.01; *** p < 0.001).

    Journal: Theranostics

    Article Title: Effective control of tumor growth through spatial and temporal control of theranostic sodium iodide symporter ( NIS ) gene expression using a heat-inducible gene promoter in engineered mesenchymal stem cells

    doi: 10.7150/thno.41489

    Figure Lengend Snippet: Heat-induced MSC-mediated NIS gene therapy in vivo. Three days after systemic injections of HSP70B-NIS-MSCs (black arrows), hyperthermia (red arrows) was administered to mice harboring HuH7 xenograft tumors. 12 to 18 h later, 55.5 MBq of therapeutic 131 I (green arrows) was applied. This treatment cycle was repeated for a total of three times ( A ). Tumor growth ( B ) and overall survival ( C ) were evaluated for the treatment with HSP70B-NIS-MSCs, hyperthermia and 131 I (HSP-NIS-MSCs + 41 °C + 131 I; n = 9), compared to control groups, receiving hyperthermia and saline (NaCl + 41 °C + NaCl; n = 10) and to normothermic groups (HSP70B-NIS-MSCs + 37 °C + 131 I; n = 9 and NaCl + 37 °C + NaCl; n = 10). Results are expressed as mean ± SEM (one-way ANOVA for tumor growth and log-rank test for Kaplan-Meier survival plots; * p < 0.05; ** p < 0.01; *** p < 0.001).

    Article Snippet: The human hepatocellular carcinoma (HCC) cell line HuH7 (JCRB0403; Japanese Collection of Research Bioresources Cell Bank, Osaka, Japan) was grown in Dulbecco's Modified Eagle Medium (1 g/l glucose; Sigma Aldrich, St. Louis, Missouri, USA) supplemented with 10% (v/v) fetal bovine serum (FBS; FBS Superior, Biochrom GmbH, Berlin, Germany) and 100 U/ml penicillin and 100 μg/ml streptomycin (P/S; Sigma-Aldrich).

    Techniques: In Vivo, Control, Saline