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huh7 human hepatocellular carcinoma cell lines  (ATCC)


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    ATCC huh7 human hepatocellular carcinoma cell lines
    Huh7 Human Hepatocellular Carcinoma Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 3826 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+hepatocellular+carcinoma+huh7/Hep+G2%3B+Hepatocellular%3B+Carcinoma%3B+Human/pm41733721-29-12-22
    Average 99 stars, based on 3826 article reviews
    huh7 human hepatocellular carcinoma cell lines - by Bioz Stars, 2026-10
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    Planar Chromatography:

    Article Title: Catechol inhibits epidermal growth factor-induced epithelial-to-mesenchymal transition and stem cell-like properties in hepatocellular carcinoma cells
    Article Snippet: Horseradish peroxidase-conjugated anti-mouse or anti-rabbit antibodies were obtained from Santa Cruz Biotechnology (Dallas, TX). .. Human hepatocellular carcinoma Huh7 and PLC/PRF cells were purchased from American Type Culture Collection (Manassas, VA). .. These cells were grown in RPMI-1640 medium (Hyclone, Logan, UT) containing 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin (Hyclone, Logan, UT).

    Clinical Proteomics:

    Article Title: Glucocorticoid receptor positively regulates transcription of FNDC5 in the liver
    Article Snippet: .. Human adult cardiomyocyte AC16 cells, human hepatocellular carcinoma Huh7, HepG2, Sk-Hep1, and SNU449 cells (ATCC), adenocarcinomic human alveolar basal epithelial cells A549, Plasma cell myeloma cell KMS26, cervical adenocarcinoma cell HeLa, nontumorigenic human aortic endothelial cell (HAEC) and nontumorigenic immortalized human hepatocyte cell line (MIHA) were used for this study. ..



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    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.
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    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.
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    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.
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    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.
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    ATCC human hepatocellular carcinoma cells huh7
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    Microbiome-derived metabolites spermine and sphingosine enhance sorafenib efficacy in hepatocellular carcinoma. (A) Sorafenib was administered to HCC HepG2, Huh7, and SK-Hep-1 cells. The cell viability percentage was plotted after 48 hours of treatment. The GI 50 value in each cell line was calculated based on the viability assay. (B) Cell viability was visualized as a heatmap after HepG2, Huh7, and SK-Hep-1 cells were treated with sorafenib (at the GI 50 concentration for each cell line) and each of 220 microbiome-derived metabolites from a library at the concentration of 10 µM. The intensity was % of survival and ranged from 0 to 100. Spermine (C) and sphingosine (D) were administered to HepG2, Huh7, and SK-Hep-1 cells. The percentage of cell viability was plotted after 48 hours of treatment. The GI 20 , GI 30 , and GI 50 values for each inhibitor in each cell line were calculated based on the viability assay. * p < 0.05; ** p < 0.01; *** p < 0.001 compared with control. Data are presented as the mean ± SD.

    Journal: International Journal of Biological Sciences

    Article Title: Combining sorafenib with spermine and sphingosine synergistically enhances anticancer efficacy by modulating metabolic pathways and gut microbiome in hepatocellular carcinoma

    doi: 10.7150/ijbs.118753

    Figure Lengend Snippet: Microbiome-derived metabolites spermine and sphingosine enhance sorafenib efficacy in hepatocellular carcinoma. (A) Sorafenib was administered to HCC HepG2, Huh7, and SK-Hep-1 cells. The cell viability percentage was plotted after 48 hours of treatment. The GI 50 value in each cell line was calculated based on the viability assay. (B) Cell viability was visualized as a heatmap after HepG2, Huh7, and SK-Hep-1 cells were treated with sorafenib (at the GI 50 concentration for each cell line) and each of 220 microbiome-derived metabolites from a library at the concentration of 10 µM. The intensity was % of survival and ranged from 0 to 100. Spermine (C) and sphingosine (D) were administered to HepG2, Huh7, and SK-Hep-1 cells. The percentage of cell viability was plotted after 48 hours of treatment. The GI 20 , GI 30 , and GI 50 values for each inhibitor in each cell line were calculated based on the viability assay. * p < 0.05; ** p < 0.01; *** p < 0.001 compared with control. Data are presented as the mean ± SD.

    Article Snippet: Human hepatocellular carcinoma Huh7, SK-Hep-1, and HepG2 cells were purchased from KCLB (Seoul, Korea).

    Techniques: Derivative Assay, Viability Assay, Concentration Assay, Control

    Combining sorafenib with spermine or sphingosine produces synergistic anticancer effects in advanced hepatocellular carcinoma. HepG2 (A-C) , Huh7 (D-F) , and SK-Hep-1 (G-I) cells were treated with the microbiome-derived metabolites spermine (Sper) or sphingosine (Sphi) at their GI 20 or GI 30 concentrations and different concentrations of sorafenib (Sora) for 48 hours. Using Compusyn software, the combination effects in HepG2 (B) , Huh7 (E) , and SK-Hep-1 (F) cells were calculated and displayed as the combination index (CI). Fa, Fraction affected. Using SynergyFinder software the combination effects in HepG2 (C) , Huh7 (F) , and SK-Hep-1 (I) cells were visualized. Student's t -test (*) or a two-way ANOVA (#) was performed to determine statistical significance. p < 0.05; **, p < 0.01; ***, p < 0.001 compared with control; #, p < 0.05; ##, p < 0.01 compared with the indicated group. Data are presented as the mean ± SD.

    Journal: International Journal of Biological Sciences

    Article Title: Combining sorafenib with spermine and sphingosine synergistically enhances anticancer efficacy by modulating metabolic pathways and gut microbiome in hepatocellular carcinoma

    doi: 10.7150/ijbs.118753

    Figure Lengend Snippet: Combining sorafenib with spermine or sphingosine produces synergistic anticancer effects in advanced hepatocellular carcinoma. HepG2 (A-C) , Huh7 (D-F) , and SK-Hep-1 (G-I) cells were treated with the microbiome-derived metabolites spermine (Sper) or sphingosine (Sphi) at their GI 20 or GI 30 concentrations and different concentrations of sorafenib (Sora) for 48 hours. Using Compusyn software, the combination effects in HepG2 (B) , Huh7 (E) , and SK-Hep-1 (F) cells were calculated and displayed as the combination index (CI). Fa, Fraction affected. Using SynergyFinder software the combination effects in HepG2 (C) , Huh7 (F) , and SK-Hep-1 (I) cells were visualized. Student's t -test (*) or a two-way ANOVA (#) was performed to determine statistical significance. p < 0.05; **, p < 0.01; ***, p < 0.001 compared with control; #, p < 0.05; ##, p < 0.01 compared with the indicated group. Data are presented as the mean ± SD.

    Article Snippet: Human hepatocellular carcinoma Huh7, SK-Hep-1, and HepG2 cells were purchased from KCLB (Seoul, Korea).

    Techniques: Derivative Assay, Software, Control

    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

    Fig. 4. Daidzin exerts antiviral effects on other DENV serotypes and cell lines. (A) The copy numbers of DENV-3 NS5 in BHK-21 cells. (B) The cytotoxicity of daidzin in Huh7 and Vero cells. (C-E) The RNA copies number of E and NS1 and DENV-2 induced plaques under daidzin treatment in Huh7 cells. (F) The protein levels of E and NS5 in Huh7 cells. (G-I) The RNA copies number of E and NS1 and DENV-2 induced plaques in Vero cells. (J) The protein levels of E and NS5 in Vero cells. *P < 0.05, **P < 0.01, ***P < 0.001 versus the DENV-2 group.

    Journal: Industrial Crops and Products

    Article Title: Daidzin protects against dengue virus infection by targeting viral envelope protein

    doi: 10.1016/j.indcrop.2025.120658

    Figure Lengend Snippet: Fig. 4. Daidzin exerts antiviral effects on other DENV serotypes and cell lines. (A) The copy numbers of DENV-3 NS5 in BHK-21 cells. (B) The cytotoxicity of daidzin in Huh7 and Vero cells. (C-E) The RNA copies number of E and NS1 and DENV-2 induced plaques under daidzin treatment in Huh7 cells. (F) The protein levels of E and NS5 in Huh7 cells. (G-I) The RNA copies number of E and NS1 and DENV-2 induced plaques in Vero cells. (J) The protein levels of E and NS5 in Vero cells. *P < 0.05, **P < 0.01, ***P < 0.001 versus the DENV-2 group.

    Article Snippet: Baby hamster kidney fibroblasts BHK-21, Aedes albopictus larva cells C6/36, Human hepatocellular carcinoma cells Huh7, and African green monkey kidney cells Vero were purchased from the American Type Culture Collection (Rockville, MD, USA).

    Techniques: