hcc cell lines huh7  (ATCC)


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    Structured Review

    ATCC hcc cell lines huh7
    Melatonin enhanced the sensitivity of <t>HCC</t> cells to chemotherapy by inducing lncRNA RAD51-AS1 expression. ( A – C ) The effects of melatonin combined with etoposide (VP16) on <t>Huh7</t> and HepG2 cell proliferation, migration and invasion with/without treatment with RAD51-AS1 siRNA (50 nM). p
    Hcc Cell Lines Huh7, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair"

    Article Title: Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair

    Journal: Cancers

    doi: 10.3390/cancers10090320

    Melatonin enhanced the sensitivity of HCC cells to chemotherapy by inducing lncRNA RAD51-AS1 expression. ( A – C ) The effects of melatonin combined with etoposide (VP16) on Huh7 and HepG2 cell proliferation, migration and invasion with/without treatment with RAD51-AS1 siRNA (50 nM). p
    Figure Legend Snippet: Melatonin enhanced the sensitivity of HCC cells to chemotherapy by inducing lncRNA RAD51-AS1 expression. ( A – C ) The effects of melatonin combined with etoposide (VP16) on Huh7 and HepG2 cell proliferation, migration and invasion with/without treatment with RAD51-AS1 siRNA (50 nM). p

    Techniques Used: Expressing, Migration

    Melatonin suppressed proliferation, migration and invasion capacities in HCC cells. ( A ) Huh7 and HepG2 cells were treated with 1 mM melatonin, and cell proliferation capacity was assessed at the indicated time points using an xCELLigence real-time cell analyzer. Mock: cells treated with DMEM medium. Vehicle: cells treated with DMSO. p
    Figure Legend Snippet: Melatonin suppressed proliferation, migration and invasion capacities in HCC cells. ( A ) Huh7 and HepG2 cells were treated with 1 mM melatonin, and cell proliferation capacity was assessed at the indicated time points using an xCELLigence real-time cell analyzer. Mock: cells treated with DMEM medium. Vehicle: cells treated with DMSO. p

    Techniques Used: Migration

    Melatonin suppressed the DNA repair capacity of HCC cells by inhibiting RAD51 expression. ( A ) A comet assay shows DNA repair activity after treatment with melatonin. Huh7 cells were treated with 200 µM etoposide (VP16) for 1 h, followed by treatment with different concentrations of melatonin in etoposide-free medium for 4 h. The cells were harvested and subjected to comet assays to detect DNA repair activity. The rows of panels present the results of three individual experiments. Quantification of cell repair activity is shown in ( B ). p
    Figure Legend Snippet: Melatonin suppressed the DNA repair capacity of HCC cells by inhibiting RAD51 expression. ( A ) A comet assay shows DNA repair activity after treatment with melatonin. Huh7 cells were treated with 200 µM etoposide (VP16) for 1 h, followed by treatment with different concentrations of melatonin in etoposide-free medium for 4 h. The cells were harvested and subjected to comet assays to detect DNA repair activity. The rows of panels present the results of three individual experiments. Quantification of cell repair activity is shown in ( B ). p

    Techniques Used: Expressing, Single Cell Gel Electrophoresis, Activity Assay

    Melatonin enhanced the sensitivity of HCC cells to chemotherapy and radiotherapy. ( A ) The proliferation capacity of Huh7 and HepG2 cells treated with 1 mM melatonin, 200 µM etoposide (VP16), or both was monitored using an xCELLigence real-time cell analyzer. p
    Figure Legend Snippet: Melatonin enhanced the sensitivity of HCC cells to chemotherapy and radiotherapy. ( A ) The proliferation capacity of Huh7 and HepG2 cells treated with 1 mM melatonin, 200 µM etoposide (VP16), or both was monitored using an xCELLigence real-time cell analyzer. p

    Techniques Used:

    2) Product Images from "RRAD suppresses the Warburg effect by downregulating ACTG1 in hepatocellular carcinoma"

    Article Title: RRAD suppresses the Warburg effect by downregulating ACTG1 in hepatocellular carcinoma

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S197844

    Effect of ACTG1 on the proliferation and cell cycle of HCC cells. Notes: ( A , B ) Cell viability was enhanced/decreased when ACTG1 was overexpressed/knocked down. ( C , D ) EdU assays showed that cell proliferation was enhanced/ decreased when ACTG1 was overexpressed/knocked down. Arrows indicate cells with high viability. All the cells can be identified by Hoechst in blue and cells with high viability can be identified by EdU in red. Cells with high viability are pink when merged. ( E , F ) Cell cycle analysis for SK-Hep-1 cells treated with NC or ACTG1 lentivirus/ Huh7 cells transfected with NC or ACTG1 shRNAs. ( G ) Expression of cyclin A2/D1/E1 and CDK2/4 was upregulated/downregulated when ACTG1 was overexpressed/ knocked down. * P
    Figure Legend Snippet: Effect of ACTG1 on the proliferation and cell cycle of HCC cells. Notes: ( A , B ) Cell viability was enhanced/decreased when ACTG1 was overexpressed/knocked down. ( C , D ) EdU assays showed that cell proliferation was enhanced/ decreased when ACTG1 was overexpressed/knocked down. Arrows indicate cells with high viability. All the cells can be identified by Hoechst in blue and cells with high viability can be identified by EdU in red. Cells with high viability are pink when merged. ( E , F ) Cell cycle analysis for SK-Hep-1 cells treated with NC or ACTG1 lentivirus/ Huh7 cells transfected with NC or ACTG1 shRNAs. ( G ) Expression of cyclin A2/D1/E1 and CDK2/4 was upregulated/downregulated when ACTG1 was overexpressed/ knocked down. * P

    Techniques Used: Cell Cycle Assay, Transfection, Expressing

    3) Product Images from "Downregulation of P-cadherin expression in hepatocellular carcinoma induces tumorigenicity"

    Article Title: Downregulation of P-cadherin expression in hepatocellular carcinoma induces tumorigenicity

    Journal: International Journal of Clinical and Experimental Pathology

    doi:

    P-cadherin expression in HCC cells and tissues. A. Quantitative realtime RT-PCR of P-cadherin expression in primary human hepatocytes (PHH) of three different donors and four HCC cell lines (HepG2, PLC, Huh7 and Hep3B) (*: P
    Figure Legend Snippet: P-cadherin expression in HCC cells and tissues. A. Quantitative realtime RT-PCR of P-cadherin expression in primary human hepatocytes (PHH) of three different donors and four HCC cell lines (HepG2, PLC, Huh7 and Hep3B) (*: P

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Planar Chromatography

    4) Product Images from "Ubiquitin-specific protease 4 promotes hepatocellular carcinoma progression via cyclophilin A stabilization and deubiquitination"

    Article Title: Ubiquitin-specific protease 4 promotes hepatocellular carcinoma progression via cyclophilin A stabilization and deubiquitination

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-017-0182-5

    USP4 stabilizes and protects CypA from degradation via deubiquitination. a Different forced USP4 expression affected the protein levels of CypA, whereas regulated expression of CypA had no effect on USP4 protein levels. b CypA was not regulated by USP4 at the mRNA level. c , d USP4 overexpression increased CypA protein levels endogenously and exogenously in Huh7 cells. USP4 knockdown decreased CypA protein levels endogenously and exogenously in MHCC97H cells. e Impact of USP4 on CypA ubiquitination in vivo. Lysates of 293T cells were immunoprecipitated with an antibody against Flag-tag and analyzed using western blotting analyses to detect poly-ubiquitination of CypA. f The impact of USP4 on CypA ubiquitination in MHCC97H cells. Lysates of MHCC97H cells with USP4-shRNA transfected or not were immunoprecipitated with an antibody against Flag-tag and analyzed using western blotting analyses to detect poly-ubiquitination of CypA. g USP4 enhanced stability of the CypA protein. MHCC97H-pLKO/shUSP4 cells and Huh7-USP4/vector cells were exposed to CHX and collected at the indicated times. Expression of CypA was examined using western blotting assays. The experiments were repeated three times. Western blotting analyses were quantified via densitometry. Error bars represent the SD. ** P
    Figure Legend Snippet: USP4 stabilizes and protects CypA from degradation via deubiquitination. a Different forced USP4 expression affected the protein levels of CypA, whereas regulated expression of CypA had no effect on USP4 protein levels. b CypA was not regulated by USP4 at the mRNA level. c , d USP4 overexpression increased CypA protein levels endogenously and exogenously in Huh7 cells. USP4 knockdown decreased CypA protein levels endogenously and exogenously in MHCC97H cells. e Impact of USP4 on CypA ubiquitination in vivo. Lysates of 293T cells were immunoprecipitated with an antibody against Flag-tag and analyzed using western blotting analyses to detect poly-ubiquitination of CypA. f The impact of USP4 on CypA ubiquitination in MHCC97H cells. Lysates of MHCC97H cells with USP4-shRNA transfected or not were immunoprecipitated with an antibody against Flag-tag and analyzed using western blotting analyses to detect poly-ubiquitination of CypA. g USP4 enhanced stability of the CypA protein. MHCC97H-pLKO/shUSP4 cells and Huh7-USP4/vector cells were exposed to CHX and collected at the indicated times. Expression of CypA was examined using western blotting assays. The experiments were repeated three times. Western blotting analyses were quantified via densitometry. Error bars represent the SD. ** P

    Techniques Used: Expressing, Over Expression, In Vivo, Immunoprecipitation, FLAG-tag, Western Blot, shRNA, Transfection, Plasmid Preparation

    CypA is indispensable for the oncogenic role of USP4. a , b The effects of CypA on USP4-induced proliferation were investigated in HCC cells using CCK-8 assays. Statistical analyses were determined using one-way ANOVA. ** P
    Figure Legend Snippet: CypA is indispensable for the oncogenic role of USP4. a , b The effects of CypA on USP4-induced proliferation were investigated in HCC cells using CCK-8 assays. Statistical analyses were determined using one-way ANOVA. ** P

    Techniques Used: CCK-8 Assay

    High expression of USP4 in HCC tissues and clinical significance. a USP4 mRNA levels in microarray datasets from Oncomine Database, Chen Liver. b qRT-PCR detection of USP4 expression in 30 paired specimens of HCC tissues and matched adjacent non-tumorous liver tissues. c Western blotting analysis of USP4 expression in six paired specimens randomly selected. T HCC tissues; N corresponding normal tissues. GAPDH was used as the loading control. d IHC analysis and staining scores of USP4 expression in 80 pairs of HCC and matched non-tumor tissues. Representative images of different USP4 expression levels are shown. Scale bars ×100: 200μm, Scale bars ×200: 100μm. e Kaplan–Meier analysis with log-rank testing of survival was performed in HCC patients with different USP4 expression levels. Error bars represent the SD. * P
    Figure Legend Snippet: High expression of USP4 in HCC tissues and clinical significance. a USP4 mRNA levels in microarray datasets from Oncomine Database, Chen Liver. b qRT-PCR detection of USP4 expression in 30 paired specimens of HCC tissues and matched adjacent non-tumorous liver tissues. c Western blotting analysis of USP4 expression in six paired specimens randomly selected. T HCC tissues; N corresponding normal tissues. GAPDH was used as the loading control. d IHC analysis and staining scores of USP4 expression in 80 pairs of HCC and matched non-tumor tissues. Representative images of different USP4 expression levels are shown. Scale bars ×100: 200μm, Scale bars ×200: 100μm. e Kaplan–Meier analysis with log-rank testing of survival was performed in HCC patients with different USP4 expression levels. Error bars represent the SD. * P

    Techniques Used: Expressing, Microarray, Quantitative RT-PCR, Western Blot, Immunohistochemistry, Staining

    High USP4 expression promoted HCC cells growth and migration in vitro. a qRT-PCR and western blotting assays were used to detect the USP4 expression in eight HCC cell lines. The statistical analyses compared Huh7, PLC/PRF/5, and Hep3B cell lines with other HCC cell lines by using one-way ANOVA. b Cell proliferation in HCC cells with regulated USP4 expression was assessed by using CCK-8 assays. c Colony formation assays were performed in HCC cells with different levels of forced USP4 expression. The number of colonies was quantified. d Apoptosis in HCC cells with forced USP4 expression was assessed using FCM. UR+LR percentage represents the apoptosis rate. Western blotting assays were used to investigate expression of cell apoptosis indicator proteins. c-PARP, cleaved-PARP. c-caspase3, cleaved-caspase3. e The in vitro migration abilities of HCC cells with different forced USP4 expression were assessed using transwell assays. Representative images are shown. f Wound healing assays were performed to evaluate the migration of HCC cells with different forced USP4 expression. Cells were cultured in FBS-free medium in the experimental period and wound closure percentage was calculated. Each experiment was repeated three times. Error bars represent the SD. The statistical analyses compared the experimental group and the control group. * P
    Figure Legend Snippet: High USP4 expression promoted HCC cells growth and migration in vitro. a qRT-PCR and western blotting assays were used to detect the USP4 expression in eight HCC cell lines. The statistical analyses compared Huh7, PLC/PRF/5, and Hep3B cell lines with other HCC cell lines by using one-way ANOVA. b Cell proliferation in HCC cells with regulated USP4 expression was assessed by using CCK-8 assays. c Colony formation assays were performed in HCC cells with different levels of forced USP4 expression. The number of colonies was quantified. d Apoptosis in HCC cells with forced USP4 expression was assessed using FCM. UR+LR percentage represents the apoptosis rate. Western blotting assays were used to investigate expression of cell apoptosis indicator proteins. c-PARP, cleaved-PARP. c-caspase3, cleaved-caspase3. e The in vitro migration abilities of HCC cells with different forced USP4 expression were assessed using transwell assays. Representative images are shown. f Wound healing assays were performed to evaluate the migration of HCC cells with different forced USP4 expression. Cells were cultured in FBS-free medium in the experimental period and wound closure percentage was calculated. Each experiment was repeated three times. Error bars represent the SD. The statistical analyses compared the experimental group and the control group. * P

    Techniques Used: Expressing, Migration, In Vitro, Quantitative RT-PCR, Western Blot, Planar Chromatography, CCK-8 Assay, Cell Culture

    USP4 interacts with CypA. a Identification of USP4 binding partners using a combination of Co-IP and high-resolution LC-MS/MS analysis. The Venn diagram shows the number of binding partners of USP4 in the two groups. Nine overlapping proteins with a ratio of > 2 are list. APC average peptide count, OE overexpression. b Western blotting assays were used to detect CypA expression in eight HCC cell lines and a normal liver cell line, LO2. Spearman correlation analysis was performed on the protein levels of USP4 and CypA in the eight HCC cell lines. c Western blotting analysis of lysates after Co-IP assays from MHCC97H cells to validate the endogenous formation of the USP4/CypA complex. d Western blotting analysis of lysates after Co-IP assays from 293T cells transfected with Myc-USP4 and Flag-CypA plasmids to validate exogenous USP4/CypA complex formation. e GST-CypA fusion protein was incubated with GST-beads and lysates of USP4 transfected 293T cells. The interacting USP4 was probed using western blotting. f Immunofluorescence staining was used to observe the expression of USP4 and CypA in MHCC97H and Huh7 cells. Representative images are shown. Scale bars: 10μm
    Figure Legend Snippet: USP4 interacts with CypA. a Identification of USP4 binding partners using a combination of Co-IP and high-resolution LC-MS/MS analysis. The Venn diagram shows the number of binding partners of USP4 in the two groups. Nine overlapping proteins with a ratio of > 2 are list. APC average peptide count, OE overexpression. b Western blotting assays were used to detect CypA expression in eight HCC cell lines and a normal liver cell line, LO2. Spearman correlation analysis was performed on the protein levels of USP4 and CypA in the eight HCC cell lines. c Western blotting analysis of lysates after Co-IP assays from MHCC97H cells to validate the endogenous formation of the USP4/CypA complex. d Western blotting analysis of lysates after Co-IP assays from 293T cells transfected with Myc-USP4 and Flag-CypA plasmids to validate exogenous USP4/CypA complex formation. e GST-CypA fusion protein was incubated with GST-beads and lysates of USP4 transfected 293T cells. The interacting USP4 was probed using western blotting. f Immunofluorescence staining was used to observe the expression of USP4 and CypA in MHCC97H and Huh7 cells. Representative images are shown. Scale bars: 10μm

    Techniques Used: Binding Assay, Co-Immunoprecipitation Assay, Liquid Chromatography with Mass Spectroscopy, Over Expression, Western Blot, Expressing, Transfection, Incubation, Immunofluorescence, Staining

    USP4 promoted HCC cell growth and intrahepatic metastasis in vivo. a USP4 knockdown suppressed HCC cell tumorigenesis in vivo ( n = 6). The volume of subcutaneous tumors was measured. b IHC staining of xenograft tumors for the cell proliferation biomarker, Ki-67, derived from MHCC97H-shUSP4 cells and control cells. Representative images are shown. c Representative images of intrahepatic metastatic nodules derived from stable MHCC97H-shUSP4 cells and control cells are shown ( n = 6). d USP4 overexpression promoted cell tumorigenesis in vivo ( n = 6). e Representative images of IHC staining of xenograft tumors for Ki-67 derived from Huh7-USP4 cells and control cells are shown. Error bars represent the SD. * P
    Figure Legend Snippet: USP4 promoted HCC cell growth and intrahepatic metastasis in vivo. a USP4 knockdown suppressed HCC cell tumorigenesis in vivo ( n = 6). The volume of subcutaneous tumors was measured. b IHC staining of xenograft tumors for the cell proliferation biomarker, Ki-67, derived from MHCC97H-shUSP4 cells and control cells. Representative images are shown. c Representative images of intrahepatic metastatic nodules derived from stable MHCC97H-shUSP4 cells and control cells are shown ( n = 6). d USP4 overexpression promoted cell tumorigenesis in vivo ( n = 6). e Representative images of IHC staining of xenograft tumors for Ki-67 derived from Huh7-USP4 cells and control cells are shown. Error bars represent the SD. * P

    Techniques Used: In Vivo, Immunohistochemistry, Staining, Biomarker Assay, Derivative Assay, Over Expression

    5) Product Images from "Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair"

    Article Title: Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair

    Journal: Cancers

    doi: 10.3390/cancers10090320

    Melatonin induced expression of lncRNA RAD51-AS1, causing RAD51 downregulation. ( A , B ) Huh7 and HepG2 cells were treated with 1 mM melatonin for 48 h, and expression of RAD51-AS1 and RAD51 was examined by quantitative real-time RT-PCR. p
    Figure Legend Snippet: Melatonin induced expression of lncRNA RAD51-AS1, causing RAD51 downregulation. ( A , B ) Huh7 and HepG2 cells were treated with 1 mM melatonin for 48 h, and expression of RAD51-AS1 and RAD51 was examined by quantitative real-time RT-PCR. p

    Techniques Used: Expressing, Quantitative RT-PCR

    Melatonin enhanced the sensitivity of HCC cells to chemotherapy by inducing lncRNA RAD51-AS1 expression. ( A – C ) The effects of melatonin combined with etoposide (VP16) on Huh7 and HepG2 cell proliferation, migration and invasion with/without treatment with RAD51-AS1 siRNA (50 nM). p
    Figure Legend Snippet: Melatonin enhanced the sensitivity of HCC cells to chemotherapy by inducing lncRNA RAD51-AS1 expression. ( A – C ) The effects of melatonin combined with etoposide (VP16) on Huh7 and HepG2 cell proliferation, migration and invasion with/without treatment with RAD51-AS1 siRNA (50 nM). p

    Techniques Used: Expressing, Migration

    Melatonin suppressed proliferation, migration and invasion capacities in HCC cells. ( A ) Huh7 and HepG2 cells were treated with 1 mM melatonin, and cell proliferation capacity was assessed at the indicated time points using an xCELLigence real-time cell analyzer. Mock: cells treated with DMEM medium. Vehicle: cells treated with DMSO. p
    Figure Legend Snippet: Melatonin suppressed proliferation, migration and invasion capacities in HCC cells. ( A ) Huh7 and HepG2 cells were treated with 1 mM melatonin, and cell proliferation capacity was assessed at the indicated time points using an xCELLigence real-time cell analyzer. Mock: cells treated with DMEM medium. Vehicle: cells treated with DMSO. p

    Techniques Used: Migration

    Melatonin suppressed the DNA repair capacity of HCC cells by inhibiting RAD51 expression. ( A ) A comet assay shows DNA repair activity after treatment with melatonin. Huh7 cells were treated with 200 µM etoposide (VP16) for 1 h, followed by treatment with different concentrations of melatonin in etoposide-free medium for 4 h. The cells were harvested and subjected to comet assays to detect DNA repair activity. The rows of panels present the results of three individual experiments. Quantification of cell repair activity is shown in ( B ). p
    Figure Legend Snippet: Melatonin suppressed the DNA repair capacity of HCC cells by inhibiting RAD51 expression. ( A ) A comet assay shows DNA repair activity after treatment with melatonin. Huh7 cells were treated with 200 µM etoposide (VP16) for 1 h, followed by treatment with different concentrations of melatonin in etoposide-free medium for 4 h. The cells were harvested and subjected to comet assays to detect DNA repair activity. The rows of panels present the results of three individual experiments. Quantification of cell repair activity is shown in ( B ). p

    Techniques Used: Expressing, Single Cell Gel Electrophoresis, Activity Assay

    Melatonin enhanced the sensitivity of HCC cells to chemotherapy and radiotherapy. ( A ) The proliferation capacity of Huh7 and HepG2 cells treated with 1 mM melatonin, 200 µM etoposide (VP16), or both was monitored using an xCELLigence real-time cell analyzer. p
    Figure Legend Snippet: Melatonin enhanced the sensitivity of HCC cells to chemotherapy and radiotherapy. ( A ) The proliferation capacity of Huh7 and HepG2 cells treated with 1 mM melatonin, 200 µM etoposide (VP16), or both was monitored using an xCELLigence real-time cell analyzer. p

    Techniques Used:

    Melatonin suppressed tumor growth and enhanced etoposide (VP16)-induced inhibitory effects on tumors in vivo. ( A , B ) A total of 5 × 10 6 Huh7 cells were injected subcutaneously into both the right and left flanks of nude mice ( n = 6, each group). Representative images show the tumor xenografts after 4 weeks. ( C ) Tumor volumes were measured three times a week and calculated using the formula: length × width 2 × 0.5. Bars indicate S.D. * p
    Figure Legend Snippet: Melatonin suppressed tumor growth and enhanced etoposide (VP16)-induced inhibitory effects on tumors in vivo. ( A , B ) A total of 5 × 10 6 Huh7 cells were injected subcutaneously into both the right and left flanks of nude mice ( n = 6, each group). Representative images show the tumor xenografts after 4 weeks. ( C ) Tumor volumes were measured three times a week and calculated using the formula: length × width 2 × 0.5. Bars indicate S.D. * p

    Techniques Used: In Vivo, Injection, Mouse Assay

    6) Product Images from "Corylin increases the sensitivity of hepatocellular carcinoma cells to chemotherapy through long noncoding RNA RAD51-AS1-mediated inhibition of DNA repair"

    Article Title: Corylin increases the sensitivity of hepatocellular carcinoma cells to chemotherapy through long noncoding RNA RAD51-AS1-mediated inhibition of DNA repair

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-018-0575-0

    Corylin increases the sensitivity of HCC cells to a chemotherapeutic agent by inducing lncRNA RAD51-AS1. a – d The effects of corylin (30 μM) combined with etoposide (VP16) (200 μM) on cell proliferation, migration, invasion, and apoptosis with/without treatment with RAD51-AS1 siRNA (50 nM) in HCC cells. * p
    Figure Legend Snippet: Corylin increases the sensitivity of HCC cells to a chemotherapeutic agent by inducing lncRNA RAD51-AS1. a – d The effects of corylin (30 μM) combined with etoposide (VP16) (200 μM) on cell proliferation, migration, invasion, and apoptosis with/without treatment with RAD51-AS1 siRNA (50 nM) in HCC cells. * p

    Techniques Used: Migration

    Corylin inhibited the growth of HCC tumors and increased the in vivo inhibitory effects of a chemotherapeutic drug on tumors. a , b A total of 4 × 10 6 Huh7 cells were inoculated into nude mice ( n = 6 each group). The mice with tumors were intraperitoneally (IP) injected 3 days per week with 100 µl of corylin (20 mg/kg of body weight), etoposide (VP16) (5 mg/kg), or an equal volume of dimethyl sulfoxide (DMSO), which served as the control. Representative images show the tumor xenografts at 4 weeks post-implantation. c The tumor volumes were calculated every 3 days after injection. The volume of each tumor was calculated as follows: length × width 2 × 0.5. The cars indicate the S.D. ** p
    Figure Legend Snippet: Corylin inhibited the growth of HCC tumors and increased the in vivo inhibitory effects of a chemotherapeutic drug on tumors. a , b A total of 4 × 10 6 Huh7 cells were inoculated into nude mice ( n = 6 each group). The mice with tumors were intraperitoneally (IP) injected 3 days per week with 100 µl of corylin (20 mg/kg of body weight), etoposide (VP16) (5 mg/kg), or an equal volume of dimethyl sulfoxide (DMSO), which served as the control. Representative images show the tumor xenografts at 4 weeks post-implantation. c The tumor volumes were calculated every 3 days after injection. The volume of each tumor was calculated as follows: length × width 2 × 0.5. The cars indicate the S.D. ** p

    Techniques Used: In Vivo, Mouse Assay, Injection

    Corylin inhibited the proliferation, migration, and invasion capacities of HCC cells. a Sensitivity of HCC cell lines to corylin treatment. Cells were treated with different concentrations of corylin for 72 h. Viability of the treated cells were assayed using an xCELLigence real-time cell analyzer. The inhibitory concentration (IC 50 ) of corylin on HCC cells was calculated by Graphpad prism 6 software. b Huh7 and HepG2 cells were treated with 30 μM corylin, and the cell proliferation capacities were monitored at the indicated time points using an xCELLigence real-time cell analyzer. *** p
    Figure Legend Snippet: Corylin inhibited the proliferation, migration, and invasion capacities of HCC cells. a Sensitivity of HCC cell lines to corylin treatment. Cells were treated with different concentrations of corylin for 72 h. Viability of the treated cells were assayed using an xCELLigence real-time cell analyzer. The inhibitory concentration (IC 50 ) of corylin on HCC cells was calculated by Graphpad prism 6 software. b Huh7 and HepG2 cells were treated with 30 μM corylin, and the cell proliferation capacities were monitored at the indicated time points using an xCELLigence real-time cell analyzer. *** p

    Techniques Used: Migration, Concentration Assay, Software

    Corylin increased the sensitivity of HCC cells to chemotherapy and radiotherapy. a The cell proliferation capacities of Huh7 (upper panel) and HepG2 (lower panel) cells with different treatments were monitored using an xCELLigence real-time cell analyzer. Data were expressed as the mean ± S.D. of three independent experiments. b Flow cytometry analysis of cell apoptosis. Huh7 cells were treated with 30 μM corylin in the presence or absence of 200 μM etoposide (VP16) for 48 h, and cell apoptosis was determined by flow cytometry after Annexin V/PI staining (left panel). The quantification of the apoptotic cells is presented in the right panel. *** p
    Figure Legend Snippet: Corylin increased the sensitivity of HCC cells to chemotherapy and radiotherapy. a The cell proliferation capacities of Huh7 (upper panel) and HepG2 (lower panel) cells with different treatments were monitored using an xCELLigence real-time cell analyzer. Data were expressed as the mean ± S.D. of three independent experiments. b Flow cytometry analysis of cell apoptosis. Huh7 cells were treated with 30 μM corylin in the presence or absence of 200 μM etoposide (VP16) for 48 h, and cell apoptosis was determined by flow cytometry after Annexin V/PI staining (left panel). The quantification of the apoptotic cells is presented in the right panel. *** p

    Techniques Used: Flow Cytometry, Staining

    Corylin induced the expression of lncRNA RAD51-AS1 to downregulate the RAD51 protein. a , b Huh7 and HepG2 cells were treated with 30 μM corylin for 48 h, and the expression of RAD51-AS1 and RAD51 was analyzed by quantitative real-time RT-PCR. GAPDH served as an internal control. *** p
    Figure Legend Snippet: Corylin induced the expression of lncRNA RAD51-AS1 to downregulate the RAD51 protein. a , b Huh7 and HepG2 cells were treated with 30 μM corylin for 48 h, and the expression of RAD51-AS1 and RAD51 was analyzed by quantitative real-time RT-PCR. GAPDH served as an internal control. *** p

    Techniques Used: Expressing, Quantitative RT-PCR

    Corylin decreased the DNA damage repair capacity of HCC cells by suppressing RAD51 expression. a Comet assays represented the activity of DNA damage repair after treatment with different concentrations of corylin. Huh7 cells were treated with 200 µM etoposide (VP16) for 1 h, followed by treatment with different concentrations of corylin in etoposide (VP16)-free medium for 4 h. The cells were harvested and subjected to comet assays to detect the DNA repair activity. The quantitative DNA damage repair activity results are shown in b . ** p
    Figure Legend Snippet: Corylin decreased the DNA damage repair capacity of HCC cells by suppressing RAD51 expression. a Comet assays represented the activity of DNA damage repair after treatment with different concentrations of corylin. Huh7 cells were treated with 200 µM etoposide (VP16) for 1 h, followed by treatment with different concentrations of corylin in etoposide (VP16)-free medium for 4 h. The cells were harvested and subjected to comet assays to detect the DNA repair activity. The quantitative DNA damage repair activity results are shown in b . ** p

    Techniques Used: Expressing, Activity Assay

    7) Product Images from "Activation of Tyrosine Metabolism in CD13+ Cancer Stem Cells Drives Relapse in Hepatocellular Carcinoma"

    Article Title: Activation of Tyrosine Metabolism in CD13+ Cancer Stem Cells Drives Relapse in Hepatocellular Carcinoma

    Journal: Cancer Research and Treatment : Official Journal of Korean Cancer Association

    doi: 10.4143/crt.2019.444

    Quiescent CD13 + cancer stem cells in hepatocellular carcinomas (HCCs) are enriched following chemotherapy. (A) HepG2 and HuH7 cells were persistently treated with 5-fluorouracil (5-FU; 5 μM) or sorafenib (SR; 4 μM) and analyzed for CD13 expression by flow cytometry at the indicated time points. Dead cells were detected by 7AAD staining. (B) Immunoblotting of CD13 protein expression in pre- and drug-treated HepG2 and HuH7 cells at 48-hour post-treatment. (C) Representative markers for proliferation were examined at the mRNA level in CD13 + and CD13 - subsets from HepG2 and HhH7 cells. (D) Cell cycle distribution of CD13 + and CD13 - fractions from HepG2 or HuH7 cells was determined by combined staining with Hoechst33342 and pyroninY. (D) Cell cycle distribution of CD13 + and CD13 - fractions from HepG2 or HuH7 cells was determined by combined staining with Hoechst33342 and pyroninY. (E) Representative images of CD13 + cell frequency in untreated tumors and tumor remnants after hepatic arterial infusion chemotherapy evaluated by immunohistochemistry (IHC). Scale bar=50 μm. (F) Comparison of IHC CD13 staining from nine HCC patients before and after hepatic arterial infusion chemotherapy. All patients achieved a partial regression. (G) Representative images of primary 3D organoids on day 12 from tumor biopsies of two HCC patients (T3 and T4). Scale bar=100 μm. (H) The representative images of T4-derived 3D organoids are shown (upper) along with the corresponding growth curve (bottom). Scale bar=150 μm. (I) Quantification analysis of CD13 + cells in primary T3/T4 tumors and their corresponding organoids. (J) Flow cytometric analysis of CD13 + cells in T3 and T4-derived organoids during serial passages. (K) Organoid-forming efficiency in the serial organoid cultures upon the administration of chemotherapeutic agents (5 μM 5-FU or 4 μM sorafenib). (L) Flow cytometric quantification analysis of CD13 + cells in the serial organoid cultures upon administration of chemotherapeutic agents (5 μM 5-FU or 4 μM SR). Values shown are mean±standard deviation. A two-tailed unpaired t test was used to compare experimental groups. *p
    Figure Legend Snippet: Quiescent CD13 + cancer stem cells in hepatocellular carcinomas (HCCs) are enriched following chemotherapy. (A) HepG2 and HuH7 cells were persistently treated with 5-fluorouracil (5-FU; 5 μM) or sorafenib (SR; 4 μM) and analyzed for CD13 expression by flow cytometry at the indicated time points. Dead cells were detected by 7AAD staining. (B) Immunoblotting of CD13 protein expression in pre- and drug-treated HepG2 and HuH7 cells at 48-hour post-treatment. (C) Representative markers for proliferation were examined at the mRNA level in CD13 + and CD13 - subsets from HepG2 and HhH7 cells. (D) Cell cycle distribution of CD13 + and CD13 - fractions from HepG2 or HuH7 cells was determined by combined staining with Hoechst33342 and pyroninY. (D) Cell cycle distribution of CD13 + and CD13 - fractions from HepG2 or HuH7 cells was determined by combined staining with Hoechst33342 and pyroninY. (E) Representative images of CD13 + cell frequency in untreated tumors and tumor remnants after hepatic arterial infusion chemotherapy evaluated by immunohistochemistry (IHC). Scale bar=50 μm. (F) Comparison of IHC CD13 staining from nine HCC patients before and after hepatic arterial infusion chemotherapy. All patients achieved a partial regression. (G) Representative images of primary 3D organoids on day 12 from tumor biopsies of two HCC patients (T3 and T4). Scale bar=100 μm. (H) The representative images of T4-derived 3D organoids are shown (upper) along with the corresponding growth curve (bottom). Scale bar=150 μm. (I) Quantification analysis of CD13 + cells in primary T3/T4 tumors and their corresponding organoids. (J) Flow cytometric analysis of CD13 + cells in T3 and T4-derived organoids during serial passages. (K) Organoid-forming efficiency in the serial organoid cultures upon the administration of chemotherapeutic agents (5 μM 5-FU or 4 μM sorafenib). (L) Flow cytometric quantification analysis of CD13 + cells in the serial organoid cultures upon administration of chemotherapeutic agents (5 μM 5-FU or 4 μM SR). Values shown are mean±standard deviation. A two-tailed unpaired t test was used to compare experimental groups. *p

    Techniques Used: Expressing, Flow Cytometry, Staining, Immunohistochemistry, Derivative Assay, Standard Deviation, Two Tailed Test

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    ATCC hcc cell lines huh7
    Melatonin enhanced the sensitivity of <t>HCC</t> cells to chemotherapy by inducing lncRNA RAD51-AS1 expression. ( A – C ) The effects of melatonin combined with etoposide (VP16) on <t>Huh7</t> and HepG2 cell proliferation, migration and invasion with/without treatment with RAD51-AS1 siRNA (50 nM). p
    Hcc Cell Lines Huh7, supplied by ATCC, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human hcc cell lines
    Gankyrin is critical for KIFC1-mediated EMT and <t>HCC</t> metastasis. a Western blot analysis of KIFC1, TWIST1, p-AKT, AKT and Gankyrin expression in <t>SMMC7721</t> and HCCLM3 cells. b Western blot analysis of Gankyrin expression after Gankyrin upregulation or silencing in HCC cells. c Protein expression in HCC cells, as determined by western blotting. Gankyrin knockdown reversed the upregulation of gankyrin, p-AKT, TWIST1, N-cadherin and vimentin levels and downregulation of E-cadherin induced by KIFC1 overexpression. Gankyrin overexpression reversed the effects of KIFC1 silencing in HCCLM3 cells. d Representative images from the Matrigel invasion assays using indicated cell lines. Gankyrin knockdown decreased the KIFC1-induced invasion of SMMC7721 cells, whereas its overexpression reversed these effects in HCCLM3 cells (200 × ). The lower panel shows the counts for invaded cells. e Bioluminescence imaging of lung metastasis in indicated groups. f Number of lung metastatic nodules in indicated groups. g Representative H E images of lung tissue samples from different groups ( n = 10/group, 40 × ). Scale bars, 250 μm. h Representative images of IHC analysis of KIFC1 and gankyrin expression in 80 HCC tissues. Scale bar, red = 200 μm, black = 50 μm. i Correlation between gankyrin and KIFC1 expression levels in 80 HCC patients. Data represent mean ± SD of three independent experiments. * P
    Human Hcc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC culture human hcc cell lines
    Overexpression of ALX4 inhibits the migration and invasion of <t>HCC</t> cells. Migration and invasion of <t>Huh7</t> (A, B) and HepG2 (C, D) cells overexpressing ALX4 were measured by Transwell assays. The assay results were quantitated by counting the migrated and invaded cells in four randomly selected areas. * p
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    ATCC hcc cell lines
    MiR-211-5p suppresses proliferation, migration and invasion of <t>HCC</t> cells by targeting ACSL4. The mRNA ( a ) and protein ( b ) expression level of ACSL4 in negative control group, transfecting miR-211-5p mimics group, transfecting siACSL4-2 group, and transfecting miR-211-5p mimics plus pcDNA3.1-ACSL4 group. c The proliferation ability of <t>LM3</t> cells in negative control group, miR-211-5p mimics group, transfecting siACSL4-2 group, and ACSL4 rescue group. d Comparison of migration and invasion of LM3 cells between negative control group, miR-211-5p mimics group, transfecting siACSL4-2 group, and ACSL4 rescue group. e Quantification analysis of results from (D). *p
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    Melatonin enhanced the sensitivity of HCC cells to chemotherapy by inducing lncRNA RAD51-AS1 expression. ( A – C ) The effects of melatonin combined with etoposide (VP16) on Huh7 and HepG2 cell proliferation, migration and invasion with/without treatment with RAD51-AS1 siRNA (50 nM). p

    Journal: Cancers

    Article Title: Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair

    doi: 10.3390/cancers10090320

    Figure Lengend Snippet: Melatonin enhanced the sensitivity of HCC cells to chemotherapy by inducing lncRNA RAD51-AS1 expression. ( A – C ) The effects of melatonin combined with etoposide (VP16) on Huh7 and HepG2 cell proliferation, migration and invasion with/without treatment with RAD51-AS1 siRNA (50 nM). p

    Article Snippet: Cell Lines, Antibodies, Drug, siRNA and Plasmid Construction The HCC cell lines Huh7 and HepG2 were purchased from American Type Culture Collection (Manassas, VA, USA), which supplies authenticated cell lines.

    Techniques: Expressing, Migration

    Melatonin suppressed proliferation, migration and invasion capacities in HCC cells. ( A ) Huh7 and HepG2 cells were treated with 1 mM melatonin, and cell proliferation capacity was assessed at the indicated time points using an xCELLigence real-time cell analyzer. Mock: cells treated with DMEM medium. Vehicle: cells treated with DMSO. p

    Journal: Cancers

    Article Title: Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair

    doi: 10.3390/cancers10090320

    Figure Lengend Snippet: Melatonin suppressed proliferation, migration and invasion capacities in HCC cells. ( A ) Huh7 and HepG2 cells were treated with 1 mM melatonin, and cell proliferation capacity was assessed at the indicated time points using an xCELLigence real-time cell analyzer. Mock: cells treated with DMEM medium. Vehicle: cells treated with DMSO. p

    Article Snippet: Cell Lines, Antibodies, Drug, siRNA and Plasmid Construction The HCC cell lines Huh7 and HepG2 were purchased from American Type Culture Collection (Manassas, VA, USA), which supplies authenticated cell lines.

    Techniques: Migration

    Melatonin suppressed the DNA repair capacity of HCC cells by inhibiting RAD51 expression. ( A ) A comet assay shows DNA repair activity after treatment with melatonin. Huh7 cells were treated with 200 µM etoposide (VP16) for 1 h, followed by treatment with different concentrations of melatonin in etoposide-free medium for 4 h. The cells were harvested and subjected to comet assays to detect DNA repair activity. The rows of panels present the results of three individual experiments. Quantification of cell repair activity is shown in ( B ). p

    Journal: Cancers

    Article Title: Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair

    doi: 10.3390/cancers10090320

    Figure Lengend Snippet: Melatonin suppressed the DNA repair capacity of HCC cells by inhibiting RAD51 expression. ( A ) A comet assay shows DNA repair activity after treatment with melatonin. Huh7 cells were treated with 200 µM etoposide (VP16) for 1 h, followed by treatment with different concentrations of melatonin in etoposide-free medium for 4 h. The cells were harvested and subjected to comet assays to detect DNA repair activity. The rows of panels present the results of three individual experiments. Quantification of cell repair activity is shown in ( B ). p

    Article Snippet: Cell Lines, Antibodies, Drug, siRNA and Plasmid Construction The HCC cell lines Huh7 and HepG2 were purchased from American Type Culture Collection (Manassas, VA, USA), which supplies authenticated cell lines.

    Techniques: Expressing, Single Cell Gel Electrophoresis, Activity Assay

    Melatonin enhanced the sensitivity of HCC cells to chemotherapy and radiotherapy. ( A ) The proliferation capacity of Huh7 and HepG2 cells treated with 1 mM melatonin, 200 µM etoposide (VP16), or both was monitored using an xCELLigence real-time cell analyzer. p

    Journal: Cancers

    Article Title: Melatonin Sensitizes Hepatocellular Carcinoma Cells to Chemotherapy Through Long Non-Coding RNA RAD51-AS1-Mediated Suppression of DNA Repair

    doi: 10.3390/cancers10090320

    Figure Lengend Snippet: Melatonin enhanced the sensitivity of HCC cells to chemotherapy and radiotherapy. ( A ) The proliferation capacity of Huh7 and HepG2 cells treated with 1 mM melatonin, 200 µM etoposide (VP16), or both was monitored using an xCELLigence real-time cell analyzer. p

    Article Snippet: Cell Lines, Antibodies, Drug, siRNA and Plasmid Construction The HCC cell lines Huh7 and HepG2 were purchased from American Type Culture Collection (Manassas, VA, USA), which supplies authenticated cell lines.

    Techniques:

    Gankyrin is critical for KIFC1-mediated EMT and HCC metastasis. a Western blot analysis of KIFC1, TWIST1, p-AKT, AKT and Gankyrin expression in SMMC7721 and HCCLM3 cells. b Western blot analysis of Gankyrin expression after Gankyrin upregulation or silencing in HCC cells. c Protein expression in HCC cells, as determined by western blotting. Gankyrin knockdown reversed the upregulation of gankyrin, p-AKT, TWIST1, N-cadherin and vimentin levels and downregulation of E-cadherin induced by KIFC1 overexpression. Gankyrin overexpression reversed the effects of KIFC1 silencing in HCCLM3 cells. d Representative images from the Matrigel invasion assays using indicated cell lines. Gankyrin knockdown decreased the KIFC1-induced invasion of SMMC7721 cells, whereas its overexpression reversed these effects in HCCLM3 cells (200 × ). The lower panel shows the counts for invaded cells. e Bioluminescence imaging of lung metastasis in indicated groups. f Number of lung metastatic nodules in indicated groups. g Representative H E images of lung tissue samples from different groups ( n = 10/group, 40 × ). Scale bars, 250 μm. h Representative images of IHC analysis of KIFC1 and gankyrin expression in 80 HCC tissues. Scale bar, red = 200 μm, black = 50 μm. i Correlation between gankyrin and KIFC1 expression levels in 80 HCC patients. Data represent mean ± SD of three independent experiments. * P

    Journal: Oncogene

    Article Title: KIFC1 regulated by miR-532-3p promotes epithelial-to-mesenchymal transition and metastasis of hepatocellular carcinoma via gankyrin/AKT signaling

    doi: 10.1038/s41388-018-0440-8

    Figure Lengend Snippet: Gankyrin is critical for KIFC1-mediated EMT and HCC metastasis. a Western blot analysis of KIFC1, TWIST1, p-AKT, AKT and Gankyrin expression in SMMC7721 and HCCLM3 cells. b Western blot analysis of Gankyrin expression after Gankyrin upregulation or silencing in HCC cells. c Protein expression in HCC cells, as determined by western blotting. Gankyrin knockdown reversed the upregulation of gankyrin, p-AKT, TWIST1, N-cadherin and vimentin levels and downregulation of E-cadherin induced by KIFC1 overexpression. Gankyrin overexpression reversed the effects of KIFC1 silencing in HCCLM3 cells. d Representative images from the Matrigel invasion assays using indicated cell lines. Gankyrin knockdown decreased the KIFC1-induced invasion of SMMC7721 cells, whereas its overexpression reversed these effects in HCCLM3 cells (200 × ). The lower panel shows the counts for invaded cells. e Bioluminescence imaging of lung metastasis in indicated groups. f Number of lung metastatic nodules in indicated groups. g Representative H E images of lung tissue samples from different groups ( n = 10/group, 40 × ). Scale bars, 250 μm. h Representative images of IHC analysis of KIFC1 and gankyrin expression in 80 HCC tissues. Scale bar, red = 200 μm, black = 50 μm. i Correlation between gankyrin and KIFC1 expression levels in 80 HCC patients. Data represent mean ± SD of three independent experiments. * P

    Article Snippet: Human HCC cell lines (Huh7, SMMC7721, HepG2, HCCLM3 and Sk-Hep-1) were purchased from the American Type Culture Collection.

    Techniques: Western Blot, Expressing, Over Expression, Imaging, Immunohistochemistry

    KIFC1 induces EMT in HCC cells. a Western blot analysis of protein expression in SMMC7721 and HCCLM3 cells. b Relative expression levels of EMT markers in SMMC7721 and HCCLM3 cells, as determined by real-time PCR. c Representative immunofluorescence images of E-cadherin and vimentin expression in indicated HCC cell lines (200 × ). Data represent mean ± SD of three independent experiments. * P

    Journal: Oncogene

    Article Title: KIFC1 regulated by miR-532-3p promotes epithelial-to-mesenchymal transition and metastasis of hepatocellular carcinoma via gankyrin/AKT signaling

    doi: 10.1038/s41388-018-0440-8

    Figure Lengend Snippet: KIFC1 induces EMT in HCC cells. a Western blot analysis of protein expression in SMMC7721 and HCCLM3 cells. b Relative expression levels of EMT markers in SMMC7721 and HCCLM3 cells, as determined by real-time PCR. c Representative immunofluorescence images of E-cadherin and vimentin expression in indicated HCC cell lines (200 × ). Data represent mean ± SD of three independent experiments. * P

    Article Snippet: Human HCC cell lines (Huh7, SMMC7721, HepG2, HCCLM3 and Sk-Hep-1) were purchased from the American Type Culture Collection.

    Techniques: Western Blot, Expressing, Real-time Polymerase Chain Reaction, Immunofluorescence

    KIFC1 promotes HCC cell migration and invasion in vitro and lung metastasis in vivo. a Results from the wound-healing assay demonstrating that KIFC1 overexpression enhanced the motility of SMMC7221-KIFC1 cells, whereas KIFC1 knockdown suppressed the motility of HCCLM3-shKIFC1 cells compared with control cells (left panel, 200 × ). Photomicrographs were obtained at 0 and 24 h and migrated distance (right panel) was measured using ImageJ software (Bethesda, USA). b Migration and invasion assays for indicated cell lines (200 × ); counts of migrated and invaded HCC cells are shown in the lower panel. c In vivo metastasis assay was performed in mice injected with stably transfected cell lines. Representative bioluminescence images and photographs of lung tumors from indicated groups are shown. d Number of lung metastatic nodules in indicated groups. e Representative H E images of lung metastases in each group ( n = 10/group, 40 × ). Scale bars, 250 μm. Data represent mean ± SD of three independent experiments. ** P

    Journal: Oncogene

    Article Title: KIFC1 regulated by miR-532-3p promotes epithelial-to-mesenchymal transition and metastasis of hepatocellular carcinoma via gankyrin/AKT signaling

    doi: 10.1038/s41388-018-0440-8

    Figure Lengend Snippet: KIFC1 promotes HCC cell migration and invasion in vitro and lung metastasis in vivo. a Results from the wound-healing assay demonstrating that KIFC1 overexpression enhanced the motility of SMMC7221-KIFC1 cells, whereas KIFC1 knockdown suppressed the motility of HCCLM3-shKIFC1 cells compared with control cells (left panel, 200 × ). Photomicrographs were obtained at 0 and 24 h and migrated distance (right panel) was measured using ImageJ software (Bethesda, USA). b Migration and invasion assays for indicated cell lines (200 × ); counts of migrated and invaded HCC cells are shown in the lower panel. c In vivo metastasis assay was performed in mice injected with stably transfected cell lines. Representative bioluminescence images and photographs of lung tumors from indicated groups are shown. d Number of lung metastatic nodules in indicated groups. e Representative H E images of lung metastases in each group ( n = 10/group, 40 × ). Scale bars, 250 μm. Data represent mean ± SD of three independent experiments. ** P

    Article Snippet: Human HCC cell lines (Huh7, SMMC7721, HepG2, HCCLM3 and Sk-Hep-1) were purchased from the American Type Culture Collection.

    Techniques: Migration, In Vitro, In Vivo, Wound Healing Assay, Over Expression, Software, Mouse Assay, Injection, Stable Transfection, Transfection

    Overexpression of ALX4 inhibits the migration and invasion of HCC cells. Migration and invasion of Huh7 (A, B) and HepG2 (C, D) cells overexpressing ALX4 were measured by Transwell assays. The assay results were quantitated by counting the migrated and invaded cells in four randomly selected areas. * p

    Journal: Oncology Research

    Article Title: Overexpression of Aristaless-Like Homeobox-4 Inhibits Proliferation, Invasion, and EMT in Hepatocellular Carcinoma Cells

    doi: 10.3727/096504016X14685034103833

    Figure Lengend Snippet: Overexpression of ALX4 inhibits the migration and invasion of HCC cells. Migration and invasion of Huh7 (A, B) and HepG2 (C, D) cells overexpressing ALX4 were measured by Transwell assays. The assay results were quantitated by counting the migrated and invaded cells in four randomly selected areas. * p

    Article Snippet: Cell Collection and Culture Human HCC cell lines (Huh7, HepG2, and HCCLM3) and normal liver cell line (L02) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Over Expression, Migration

    Overexpression of ALX4 inhibits the EMT process in HCC cells. (A) The expression of EMT-related markers E-cadherin, fibronectin, and N-cadherin in Huh7 cells overexpressing ALX4 was detected by Western blot, with β-actin as an internal control. (B) The relative protein expression levels of E-cadherin, fibronectin, and N-cadherin in the different cell groups were analyzed via Glyko BandScan 5.1 software. * p

    Journal: Oncology Research

    Article Title: Overexpression of Aristaless-Like Homeobox-4 Inhibits Proliferation, Invasion, and EMT in Hepatocellular Carcinoma Cells

    doi: 10.3727/096504016X14685034103833

    Figure Lengend Snippet: Overexpression of ALX4 inhibits the EMT process in HCC cells. (A) The expression of EMT-related markers E-cadherin, fibronectin, and N-cadherin in Huh7 cells overexpressing ALX4 was detected by Western blot, with β-actin as an internal control. (B) The relative protein expression levels of E-cadherin, fibronectin, and N-cadherin in the different cell groups were analyzed via Glyko BandScan 5.1 software. * p

    Article Snippet: Cell Collection and Culture Human HCC cell lines (Huh7, HepG2, and HCCLM3) and normal liver cell line (L02) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Over Expression, Expressing, Western Blot, Software

    Expression of ALX4 is undetectable in HCC tissues and cell lines. (A, B) qRT-PCR and Western blot assays were conducted, and the results indicated downregulation of ALX4 in HCC tissues in comparison with the matched noncancerous liver tissues. (C, D) Results of the qRT-PCR and Western blot assays showed that ALX4 was lowly expressed in three HCC cell lines (Huh7, HepG2, and HCCLM3) but was highly expressed in the normal liver cell line L02. * p

    Journal: Oncology Research

    Article Title: Overexpression of Aristaless-Like Homeobox-4 Inhibits Proliferation, Invasion, and EMT in Hepatocellular Carcinoma Cells

    doi: 10.3727/096504016X14685034103833

    Figure Lengend Snippet: Expression of ALX4 is undetectable in HCC tissues and cell lines. (A, B) qRT-PCR and Western blot assays were conducted, and the results indicated downregulation of ALX4 in HCC tissues in comparison with the matched noncancerous liver tissues. (C, D) Results of the qRT-PCR and Western blot assays showed that ALX4 was lowly expressed in three HCC cell lines (Huh7, HepG2, and HCCLM3) but was highly expressed in the normal liver cell line L02. * p

    Article Snippet: Cell Collection and Culture Human HCC cell lines (Huh7, HepG2, and HCCLM3) and normal liver cell line (L02) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot

    Overexpression of ALX4 inhibits the proliferation of HCC cells. Expression of ALX4 in Huh7 (A) and HepG2 (B) cells after transfection with pCMV-ALX4 was confirmed by Western blot assays. As shown by the MTT assay, overexpression of ALX4 obviously inhibited the proliferation rate of Huh7 (C) and HepG2 (D) cells transfected with pCMV-ALX4 compared to that of the control group transfected with pCMV-scramble. * p

    Journal: Oncology Research

    Article Title: Overexpression of Aristaless-Like Homeobox-4 Inhibits Proliferation, Invasion, and EMT in Hepatocellular Carcinoma Cells

    doi: 10.3727/096504016X14685034103833

    Figure Lengend Snippet: Overexpression of ALX4 inhibits the proliferation of HCC cells. Expression of ALX4 in Huh7 (A) and HepG2 (B) cells after transfection with pCMV-ALX4 was confirmed by Western blot assays. As shown by the MTT assay, overexpression of ALX4 obviously inhibited the proliferation rate of Huh7 (C) and HepG2 (D) cells transfected with pCMV-ALX4 compared to that of the control group transfected with pCMV-scramble. * p

    Article Snippet: Cell Collection and Culture Human HCC cell lines (Huh7, HepG2, and HCCLM3) and normal liver cell line (L02) were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Over Expression, Expressing, Transfection, Western Blot, MTT Assay

    MiR-211-5p suppresses proliferation, migration and invasion of HCC cells by targeting ACSL4. The mRNA ( a ) and protein ( b ) expression level of ACSL4 in negative control group, transfecting miR-211-5p mimics group, transfecting siACSL4-2 group, and transfecting miR-211-5p mimics plus pcDNA3.1-ACSL4 group. c The proliferation ability of LM3 cells in negative control group, miR-211-5p mimics group, transfecting siACSL4-2 group, and ACSL4 rescue group. d Comparison of migration and invasion of LM3 cells between negative control group, miR-211-5p mimics group, transfecting siACSL4-2 group, and ACSL4 rescue group. e Quantification analysis of results from (D). *p

    Journal: Journal of Translational Medicine

    Article Title: Identification of MiR-211-5p as a tumor suppressor by targeting ACSL4 in Hepatocellular Carcinoma

    doi: 10.1186/s12967-020-02494-7

    Figure Lengend Snippet: MiR-211-5p suppresses proliferation, migration and invasion of HCC cells by targeting ACSL4. The mRNA ( a ) and protein ( b ) expression level of ACSL4 in negative control group, transfecting miR-211-5p mimics group, transfecting siACSL4-2 group, and transfecting miR-211-5p mimics plus pcDNA3.1-ACSL4 group. c The proliferation ability of LM3 cells in negative control group, miR-211-5p mimics group, transfecting siACSL4-2 group, and ACSL4 rescue group. d Comparison of migration and invasion of LM3 cells between negative control group, miR-211-5p mimics group, transfecting siACSL4-2 group, and ACSL4 rescue group. e Quantification analysis of results from (D). *p

    Article Snippet: Cell culture and transfection Human hepatic cells (QSG-7701) and HCC cell lines (Huh-7, SK Hep-1, HepG2, and LM3) were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Migration, Expressing, Negative Control

    Abnormal expression and prognostic value of miR-211-5p in HCC. a The overlap miRNA among the three datasets were displayed in Venn diagram and only the hsa-miR-211-5p was the common. b Comparison of miR-211-5p expression between 30 pairs of HCC and matched adjacent tumor-free tissues from patients in clinical. c Comparison of miR-211-5p expression between HCC tissues and normal liver tissues based on TCGA cohorts. d The overall survival analysis of miR-211-5p in HCC through TCGA cohorts based on online database Kaplan–Meier Plotter. e The relative miRNA expression level of miR-211-5p in 4 HCC cell lines (Huh-7, SK Hep-1, HepG2, and LM3) compared with normal liver cells (QSG-7701). *p

    Journal: Journal of Translational Medicine

    Article Title: Identification of MiR-211-5p as a tumor suppressor by targeting ACSL4 in Hepatocellular Carcinoma

    doi: 10.1186/s12967-020-02494-7

    Figure Lengend Snippet: Abnormal expression and prognostic value of miR-211-5p in HCC. a The overlap miRNA among the three datasets were displayed in Venn diagram and only the hsa-miR-211-5p was the common. b Comparison of miR-211-5p expression between 30 pairs of HCC and matched adjacent tumor-free tissues from patients in clinical. c Comparison of miR-211-5p expression between HCC tissues and normal liver tissues based on TCGA cohorts. d The overall survival analysis of miR-211-5p in HCC through TCGA cohorts based on online database Kaplan–Meier Plotter. e The relative miRNA expression level of miR-211-5p in 4 HCC cell lines (Huh-7, SK Hep-1, HepG2, and LM3) compared with normal liver cells (QSG-7701). *p

    Article Snippet: Cell culture and transfection Human hepatic cells (QSG-7701) and HCC cell lines (Huh-7, SK Hep-1, HepG2, and LM3) were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Expressing