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hepatocellular carcinoma cell line hep3b  (DSMZ)


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    Structured Review

    DSMZ hepatocellular carcinoma cell line hep3b
    Real time monitoring of the autophagy process in untreated Hep3B cells. The cells were incubated for 48 h with complete growth medium. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.
    Hepatocellular Carcinoma Cell Line Hep3b, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 73 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hep+3b+cells/HEP-3B/pmc12887277-67-21-27
    Average 94 stars, based on 73 article reviews
    hepatocellular carcinoma cell line hep3b - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Leptin-dependent fat accumulation triggers autophagy in metabolic dysfunction-associated steatohepatitis model"

    Article Title: Leptin-dependent fat accumulation triggers autophagy in metabolic dysfunction-associated steatohepatitis model

    Journal: Translational Gastroenterology and Hepatology

    doi: 10.21037/tgh-25-17

    Real time monitoring of the autophagy process in untreated Hep3B cells. The cells were incubated for 48 h with complete growth medium. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.
    Figure Legend Snippet: Real time monitoring of the autophagy process in untreated Hep3B cells. The cells were incubated for 48 h with complete growth medium. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.

    Techniques Used:

    Real time monitoring of the autophagy process in Hep3B cells treated for 48 h with 2 mM oleic acid. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.
    Figure Legend Snippet: Real time monitoring of the autophagy process in Hep3B cells treated for 48 h with 2 mM oleic acid. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.

    Techniques Used:

    Detection of the autophagy markers in liver cancer cells. (A) RT-qPCR detection of BECN1, MAP1LC3B, SQSTM1, UVRAG, TFEB, PRKAA1_1, and PRKAA2_1 in HepG2 cells after the administration of 2 mM OA, 100 pM BAF, 2 mM caffeine and their combination. The target expression was normalized to GAPDH. Data are presented as means ± SEM of treated vs. untreated cells from three independent experiments. (B,C) Western blot detection and densitometric quantification of the protein level of Beclin1, LC3B-I, LC3B-II, UVRAG, p62, AMPK-α and P-AMPK-α. Beta-actin was detected as equal loading control and used for the further densitometric normalization of the protein level of the target proteins. The error bars of the densitometric graph represent the SEM of experiments performed in triplicates. (D) Micrographs of MAP1LC3B-GFP-RFP stably transfected Hep3B cells after the administration of 2 mM OA (scale bar =300 µm). The cells were live monitored for up to 48 h (please refer to the ). *, P<0.05 by 2-way ANOVA with Dunnett’s test (see Appendix 1 for detailed statistical analysis). ANOVA, analysis of variance; OA, oleic acid; RT-qPCR, reverse transcription quantitative polymerase chain reaction; SEM, standard error mean.
    Figure Legend Snippet: Detection of the autophagy markers in liver cancer cells. (A) RT-qPCR detection of BECN1, MAP1LC3B, SQSTM1, UVRAG, TFEB, PRKAA1_1, and PRKAA2_1 in HepG2 cells after the administration of 2 mM OA, 100 pM BAF, 2 mM caffeine and their combination. The target expression was normalized to GAPDH. Data are presented as means ± SEM of treated vs. untreated cells from three independent experiments. (B,C) Western blot detection and densitometric quantification of the protein level of Beclin1, LC3B-I, LC3B-II, UVRAG, p62, AMPK-α and P-AMPK-α. Beta-actin was detected as equal loading control and used for the further densitometric normalization of the protein level of the target proteins. The error bars of the densitometric graph represent the SEM of experiments performed in triplicates. (D) Micrographs of MAP1LC3B-GFP-RFP stably transfected Hep3B cells after the administration of 2 mM OA (scale bar =300 µm). The cells were live monitored for up to 48 h (please refer to the ). *, P<0.05 by 2-way ANOVA with Dunnett’s test (see Appendix 1 for detailed statistical analysis). ANOVA, analysis of variance; OA, oleic acid; RT-qPCR, reverse transcription quantitative polymerase chain reaction; SEM, standard error mean.

    Techniques Used: Quantitative RT-PCR, Expressing, Western Blot, Control, Stable Transfection, Transfection, Reverse Transcription, Real-time Polymerase Chain Reaction

    Autophagosome maturation monitoring in Hep3B treated with oleic acid. Intracellular lipid accumulation in HepG2 cells treated for 24 h with 500 ng/mL of rhTGF-β, 2 mM oleic acid, 100 pM bafilomycin, 2 mM caffeine and their combination. The lipids were stained with Oil Red O. Magnification: 100× (A,C) and 200× (B,D).
    Figure Legend Snippet: Autophagosome maturation monitoring in Hep3B treated with oleic acid. Intracellular lipid accumulation in HepG2 cells treated for 24 h with 500 ng/mL of rhTGF-β, 2 mM oleic acid, 100 pM bafilomycin, 2 mM caffeine and their combination. The lipids were stained with Oil Red O. Magnification: 100× (A,C) and 200× (B,D).

    Techniques Used: Staining

    Related Articles

    other:

    Article Title: P2RY2 is a purinergic immune checkpoint linking extracellular ATP to immune evasion and adaptive resistance to immunotherapy
    Article Snippet: 8505C, and HEP-3B cells were obtained from the Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH (DSMZ).

    Cell Culture:

    Article Title: Impact of Promoter Polymorphisms on the Transcriptional Regulation of the Organic Cation Transporter OCT1 (SLC22A1)
    Article Snippet: HepG2 cells (DSMZ-German Collection of Microorganisms and Cell Cultures, Braunschweig, Germany) were cultured in RPMI 1640 GlutaMAXTM-I supplemented with 10% fetal bovine serum, 100 U/mL penicillin, and 100 μg/mL streptomycin. .. Hep-3B cells (DSMZ, Braunschweig, Germany) and Huh7 cells (JCRB Cell Bank, Tokyo, Japan) were cultured in DMEM supplemented with 10% fetal bovine serum, 100 U/mL penicillin, and 100 μg/mL streptomycin. .. Cells were detached with TrypLE Express W/Phenol red (Life Technologies, Darmstadt, Germany).



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    Image Search Results


    Movie S13. FCCP treatment‐induced changes in mitochondrial morphology in Hep3B cells.

    Journal: The Febs Journal

    Article Title: Label‐free imaging of intracellular structures in living mammalian cells via external apodization phase‐contrast microscopy

    doi: 10.1111/febs.70286

    Figure Lengend Snippet: Movie S13. FCCP treatment‐induced changes in mitochondrial morphology in Hep3B cells.

    Article Snippet: Human lung carcinoma A549 cells (RRID:CVCL_0023, ATCC CCL‐185), human cervical adenocarcinoma HeLa cells (RRID:CVCL_0030, ATCC CCL‐2), human colon carcinoma HCT116 cells (RRID:CVCL_0291, ATCC CCL‐247), human hepatocellular carcinoma Hep 3B cells (RRID:CVCL_0326, ATCC HB‐8064), mouse fibroblast NIH/3T3 cells (RRID:CVCL_0594, ATCC CRL‐1658), human breast adenocarcinoma MDA‐MB‐231 cells (RRID:CVCL_0062, ATCC CRM‐HTB‐26), human osteosarcoma U2‐OS cells (RRID:CVCL_0042, ATCC HTB‐96), and human breast carcinoma ZR75‐1‐1 (RRID:CVCL_0588, ATCC CRL‐1500) cells were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques:

    Co-culture of M2 macrophage supernatant with hepatocellular carcinoma cells promotes HCC cell metastasis and EMT. ( A , B ) Wound healing assays of SNU-449 and Hep-3B cells under M0 and M2 supernatant co-culture conditions. Right panels show histogram results. Scale bar: 200 μm. ( C , D ) Transwell assays of SNU-449 and Hep-3B cells co-cultured with M0 and M2 supernatants. Scale bar: 50 μm. E Western blot analysis of EMT-related protein expression in SNU-449 and Hep-3B cells co-cultured with M0 and M2 supernatants ( n = 3 independent experiments). Data are presented as mean ± standard deviation (* P < 0.05, ** P < 0.01, *** P < 0.001 vs. Con group).

    Journal: Scientific Reports

    Article Title: Study on the effects and mechanisms of M2 macrophages on PYCR1-promoted biological behavior of hepatocellular carcinoma cells

    doi: 10.1038/s41598-026-40817-8

    Figure Lengend Snippet: Co-culture of M2 macrophage supernatant with hepatocellular carcinoma cells promotes HCC cell metastasis and EMT. ( A , B ) Wound healing assays of SNU-449 and Hep-3B cells under M0 and M2 supernatant co-culture conditions. Right panels show histogram results. Scale bar: 200 μm. ( C , D ) Transwell assays of SNU-449 and Hep-3B cells co-cultured with M0 and M2 supernatants. Scale bar: 50 μm. E Western blot analysis of EMT-related protein expression in SNU-449 and Hep-3B cells co-cultured with M0 and M2 supernatants ( n = 3 independent experiments). Data are presented as mean ± standard deviation (* P < 0.05, ** P < 0.01, *** P < 0.001 vs. Con group).

    Article Snippet: The Hep-3B cell line of human hepatocellular carcinoma was obtained from Procell (Wuhan, China), while the SNU-449 cell line was acquired from the Chinese Academy of Sciences (Shanghai, China).

    Techniques: Co-Culture Assay, Cell Culture, Western Blot, Expressing, Standard Deviation

    Knockdown of PYCR1 attenuates HCC cell metastasis and epithelial-mesenchymal transition induced by co-culture of M2 macrophage supernatant with hepatocellular carcinoma cells. ( A , B ) Wound healing assays of SNU-449 and Hep-3B cells with PYCR1 knockdown under altered co-culture conditions. Right panels show histograms of results. Scale bar: 200 μm. ( C , D ) Transwell assays assessing invasive migration of PYCR1-knockdown SNU-449 and Hep-3B cells under co-culture conditions. Scale bar: 50 μm. ( E , F ) Immunofluorescence Ki67 detection of the effect of PYCR1 knockdown on hepatocellular carcinoma cell proliferation under Co-culture Conditions ( n = 3 independent experiments). G Western blot analysis of EMT-related protein expression in PYCR1-knockdown SNU-449 and Hep-3B cells under co-culture conditions ( n = 3 independent experiments). (* P < 0.05, ** P < 0.01,*** P < 0.001, **** P < 0.0001 vs. NC + M0 group; ## P < 0.01, ### P < 0.001 vs. NC + M2 group)

    Journal: Scientific Reports

    Article Title: Study on the effects and mechanisms of M2 macrophages on PYCR1-promoted biological behavior of hepatocellular carcinoma cells

    doi: 10.1038/s41598-026-40817-8

    Figure Lengend Snippet: Knockdown of PYCR1 attenuates HCC cell metastasis and epithelial-mesenchymal transition induced by co-culture of M2 macrophage supernatant with hepatocellular carcinoma cells. ( A , B ) Wound healing assays of SNU-449 and Hep-3B cells with PYCR1 knockdown under altered co-culture conditions. Right panels show histograms of results. Scale bar: 200 μm. ( C , D ) Transwell assays assessing invasive migration of PYCR1-knockdown SNU-449 and Hep-3B cells under co-culture conditions. Scale bar: 50 μm. ( E , F ) Immunofluorescence Ki67 detection of the effect of PYCR1 knockdown on hepatocellular carcinoma cell proliferation under Co-culture Conditions ( n = 3 independent experiments). G Western blot analysis of EMT-related protein expression in PYCR1-knockdown SNU-449 and Hep-3B cells under co-culture conditions ( n = 3 independent experiments). (* P < 0.05, ** P < 0.01,*** P < 0.001, **** P < 0.0001 vs. NC + M0 group; ## P < 0.01, ### P < 0.001 vs. NC + M2 group)

    Article Snippet: The Hep-3B cell line of human hepatocellular carcinoma was obtained from Procell (Wuhan, China), while the SNU-449 cell line was acquired from the Chinese Academy of Sciences (Shanghai, China).

    Techniques: Knockdown, Co-Culture Assay, Migration, Immunofluorescence, Western Blot, Expressing

    Real time monitoring of the autophagy process in untreated Hep3B cells. The cells were incubated for 48 h with complete growth medium. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.

    Journal: Translational Gastroenterology and Hepatology

    Article Title: Leptin-dependent fat accumulation triggers autophagy in metabolic dysfunction-associated steatohepatitis model

    doi: 10.21037/tgh-25-17

    Figure Lengend Snippet: Real time monitoring of the autophagy process in untreated Hep3B cells. The cells were incubated for 48 h with complete growth medium. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.

    Article Snippet: The human hepatoblastoma cell line HepG2 (ACC180, Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures GmbH, Braunschweig, Germany), the human hepatocellular carcinoma cell line Hep3B (ACC93, DSMZ) and the human HSC line LX-2, a kindly gift from Scott Friedmann (Icahn School of Medicine at Mount Sinai), were grown in DMEM (Gibco, Paisley, UK) supplemented with 10% fetal bovine serum, penicillin (100 U/mL) and streptomycin (100 μg/mL) (11548876, Thermo Fisher Scientific, Waltham, MA, USA) at 37 °C in a humidified atmosphere containing 5% CO 2 .

    Techniques:

    Real time monitoring of the autophagy process in Hep3B cells treated for 48 h with 2 mM oleic acid. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.

    Journal: Translational Gastroenterology and Hepatology

    Article Title: Leptin-dependent fat accumulation triggers autophagy in metabolic dysfunction-associated steatohepatitis model

    doi: 10.21037/tgh-25-17

    Figure Lengend Snippet: Real time monitoring of the autophagy process in Hep3B cells treated for 48 h with 2 mM oleic acid. Hep3B cells were previously transfected with a plasmid expressing GFP-mRFP-LC3B. Green fluorescence is a marker of early autophagosomes. Instead, the red fluorescence remained stable after the fusion of the autophagosomes with lysosomes thus highlighting the late phase of autophagy.

    Article Snippet: The human hepatoblastoma cell line HepG2 (ACC180, Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures GmbH, Braunschweig, Germany), the human hepatocellular carcinoma cell line Hep3B (ACC93, DSMZ) and the human HSC line LX-2, a kindly gift from Scott Friedmann (Icahn School of Medicine at Mount Sinai), were grown in DMEM (Gibco, Paisley, UK) supplemented with 10% fetal bovine serum, penicillin (100 U/mL) and streptomycin (100 μg/mL) (11548876, Thermo Fisher Scientific, Waltham, MA, USA) at 37 °C in a humidified atmosphere containing 5% CO 2 .

    Techniques:

    Detection of the autophagy markers in liver cancer cells. (A) RT-qPCR detection of BECN1, MAP1LC3B, SQSTM1, UVRAG, TFEB, PRKAA1_1, and PRKAA2_1 in HepG2 cells after the administration of 2 mM OA, 100 pM BAF, 2 mM caffeine and their combination. The target expression was normalized to GAPDH. Data are presented as means ± SEM of treated vs. untreated cells from three independent experiments. (B,C) Western blot detection and densitometric quantification of the protein level of Beclin1, LC3B-I, LC3B-II, UVRAG, p62, AMPK-α and P-AMPK-α. Beta-actin was detected as equal loading control and used for the further densitometric normalization of the protein level of the target proteins. The error bars of the densitometric graph represent the SEM of experiments performed in triplicates. (D) Micrographs of MAP1LC3B-GFP-RFP stably transfected Hep3B cells after the administration of 2 mM OA (scale bar =300 µm). The cells were live monitored for up to 48 h (please refer to the ). *, P<0.05 by 2-way ANOVA with Dunnett’s test (see Appendix 1 for detailed statistical analysis). ANOVA, analysis of variance; OA, oleic acid; RT-qPCR, reverse transcription quantitative polymerase chain reaction; SEM, standard error mean.

    Journal: Translational Gastroenterology and Hepatology

    Article Title: Leptin-dependent fat accumulation triggers autophagy in metabolic dysfunction-associated steatohepatitis model

    doi: 10.21037/tgh-25-17

    Figure Lengend Snippet: Detection of the autophagy markers in liver cancer cells. (A) RT-qPCR detection of BECN1, MAP1LC3B, SQSTM1, UVRAG, TFEB, PRKAA1_1, and PRKAA2_1 in HepG2 cells after the administration of 2 mM OA, 100 pM BAF, 2 mM caffeine and their combination. The target expression was normalized to GAPDH. Data are presented as means ± SEM of treated vs. untreated cells from three independent experiments. (B,C) Western blot detection and densitometric quantification of the protein level of Beclin1, LC3B-I, LC3B-II, UVRAG, p62, AMPK-α and P-AMPK-α. Beta-actin was detected as equal loading control and used for the further densitometric normalization of the protein level of the target proteins. The error bars of the densitometric graph represent the SEM of experiments performed in triplicates. (D) Micrographs of MAP1LC3B-GFP-RFP stably transfected Hep3B cells after the administration of 2 mM OA (scale bar =300 µm). The cells were live monitored for up to 48 h (please refer to the ). *, P<0.05 by 2-way ANOVA with Dunnett’s test (see Appendix 1 for detailed statistical analysis). ANOVA, analysis of variance; OA, oleic acid; RT-qPCR, reverse transcription quantitative polymerase chain reaction; SEM, standard error mean.

    Article Snippet: The human hepatoblastoma cell line HepG2 (ACC180, Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures GmbH, Braunschweig, Germany), the human hepatocellular carcinoma cell line Hep3B (ACC93, DSMZ) and the human HSC line LX-2, a kindly gift from Scott Friedmann (Icahn School of Medicine at Mount Sinai), were grown in DMEM (Gibco, Paisley, UK) supplemented with 10% fetal bovine serum, penicillin (100 U/mL) and streptomycin (100 μg/mL) (11548876, Thermo Fisher Scientific, Waltham, MA, USA) at 37 °C in a humidified atmosphere containing 5% CO 2 .

    Techniques: Quantitative RT-PCR, Expressing, Western Blot, Control, Stable Transfection, Transfection, Reverse Transcription, Real-time Polymerase Chain Reaction

    Autophagosome maturation monitoring in Hep3B treated with oleic acid. Intracellular lipid accumulation in HepG2 cells treated for 24 h with 500 ng/mL of rhTGF-β, 2 mM oleic acid, 100 pM bafilomycin, 2 mM caffeine and their combination. The lipids were stained with Oil Red O. Magnification: 100× (A,C) and 200× (B,D).

    Journal: Translational Gastroenterology and Hepatology

    Article Title: Leptin-dependent fat accumulation triggers autophagy in metabolic dysfunction-associated steatohepatitis model

    doi: 10.21037/tgh-25-17

    Figure Lengend Snippet: Autophagosome maturation monitoring in Hep3B treated with oleic acid. Intracellular lipid accumulation in HepG2 cells treated for 24 h with 500 ng/mL of rhTGF-β, 2 mM oleic acid, 100 pM bafilomycin, 2 mM caffeine and their combination. The lipids were stained with Oil Red O. Magnification: 100× (A,C) and 200× (B,D).

    Article Snippet: The human hepatoblastoma cell line HepG2 (ACC180, Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures GmbH, Braunschweig, Germany), the human hepatocellular carcinoma cell line Hep3B (ACC93, DSMZ) and the human HSC line LX-2, a kindly gift from Scott Friedmann (Icahn School of Medicine at Mount Sinai), were grown in DMEM (Gibco, Paisley, UK) supplemented with 10% fetal bovine serum, penicillin (100 U/mL) and streptomycin (100 μg/mL) (11548876, Thermo Fisher Scientific, Waltham, MA, USA) at 37 °C in a humidified atmosphere containing 5% CO 2 .

    Techniques: Staining

    Promotion of HCC progression by Hp-GES-EVs through exosome-enclosed miR-362-5p. (A) miR-362-5p levels in mice serum with or without H. pylori infection. (B) RT-qPCR analysis of miR-362-5p levels in Hep G2 and Hep 3B cells co-incubated with Hp-GES-EVs. (C) Western blot analysis of TLE4 expression in Hep G2 and Hep 3B cells. (D) EdU assay showing the proliferation of Hep G2 and Hep 3B cells treated with Hp-GES-EVs and an additional miR-362-5p inhibitors. (E) Wound healing assay showing migration of Hep G2 and Hep 3B cells treated with Hp-GES-EVs and an additional miR-362-5p inhibitors. (F) serum miR-362-5p in H. pylori -infected mice with GW4869 treatment. (G) Western blot analysis of TLE4 expression in liver tissues with GW4869 treatment. Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. The scale bar represents 50 μm in (D) and 100 μm in (E) .

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: Helicobacter pylori induced miR-362-5p upregulation drives gastric cancer progression and links hepatocellular carcinoma through an exosome-dependent pathway

    doi: 10.3389/fcimb.2025.1582131

    Figure Lengend Snippet: Promotion of HCC progression by Hp-GES-EVs through exosome-enclosed miR-362-5p. (A) miR-362-5p levels in mice serum with or without H. pylori infection. (B) RT-qPCR analysis of miR-362-5p levels in Hep G2 and Hep 3B cells co-incubated with Hp-GES-EVs. (C) Western blot analysis of TLE4 expression in Hep G2 and Hep 3B cells. (D) EdU assay showing the proliferation of Hep G2 and Hep 3B cells treated with Hp-GES-EVs and an additional miR-362-5p inhibitors. (E) Wound healing assay showing migration of Hep G2 and Hep 3B cells treated with Hp-GES-EVs and an additional miR-362-5p inhibitors. (F) serum miR-362-5p in H. pylori -infected mice with GW4869 treatment. (G) Western blot analysis of TLE4 expression in liver tissues with GW4869 treatment. Data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. The scale bar represents 50 μm in (D) and 100 μm in (E) .

    Article Snippet: GES-1, HEK293, Hep G2 and Hep 3B cells were cultured in DMEM medium (Pricells, PM150210, China) supplemented with 10% (v/v) FBS (Gibco, A5669701, USA), while cells of AGS and MKN45 were cultured in RPMI 1640 (Pricells, PM150110, China) medium with 10% (v/v) FBS (Gibco).

    Techniques: Infection, Quantitative RT-PCR, Incubation, Western Blot, Expressing, EdU Assay, Wound Healing Assay, Migration