Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Increased expression of c-Jun in nonalcoholic fatty liver disease.

doi: 10.1038/labinvest.2014.3

Figure Lengend Snippet: Figure 7 c-Jun expression pattern in liver tissues of patients with NAFLD. (a) Immunohistochemical c-Jun staining of a TMA comprising 110 non- tumorous human hepatic tissue specimens with normal histology (n ¼ 38) or NAFLD (n ¼ 72) different degree of steatosis and inflammation. Representative images of livers with NAFLD and with absent (score ¼ 0; left panel), weak (score ¼ 1; middle panel) or strong (score ¼ 2; right panel) immunoreactivity for c-Jun. (b) Percental distribution of livers with absent, weak or strong immunoreactivity for c-Jun in normal and NAFLD livers. (c) Percentage of steatotic hepatocytes in livers with absent, weak or strong cytoplasmatic staining for c-Jun (*Po0.05). Comparison between the staining patterns for c-Jun and phosphorylated c-Jun in tissue specimens of NAFLD livers applying TMA technology. Representative images of a NAFLD liver stained for (d) c-Jun and (e) phosphorylated (Ser73) c-Jun. Analysis of (f) c-JUN and (g) IL-8 mRNA expression levels by quantitative RT-PCR in PHHs stimulated with indicated concentrations of the FFA palmitic acid for 24 hours (*Po0.05 compared with FFA-free control; CTR) as well. (h, i) c-JUN and IL-8 mRNA expression in Hep3B hepatoma cells transfected with c-JUN-siRNA or control-siRNA and subsequent stimulation with 0.3 mM of the FFA palmitic acid for 24 h. (*Po0.05).

Article Snippet: Cells, Cell Culture and In Vitro Experiments Primary human hepatocytes (PHHs) and hepatoma cell lines HepG2 (ATCC HB-8065) and Hep3B (ATCC HB-8064) were isolated and/or cultured as described previously.28,29 Under the same conditions, cells were stimulated with indicated concentrations of the FFA palmitic acid for 24 h using a specifically prepared palmitic acid/bovine serum albumin (BSA) stock solution.

Techniques: Expressing, Immunohistochemical staining, Staining, Comparison, Quantitative RT-PCR, Control, Transfection

Journal: International journal of oncology

Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.

doi: 10.3892/ijo.2015.3087

Figure Lengend Snippet: Figure 1. Effect of panobinostat (LBH589) on gene expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) and fms-like tyrosine kinase-1 (FLT-1) in vitro in HepG2 and Hep3B cells. (A) Quantitative real-time RT-PCR analysis after 24, 48 and 72 h treatment with 0.01 µM panobinostat (A) and 0.1 µM panobinostat (B) in HepG2 cells, with 0.01 µM panobinostat (C) and 0.1 µM panobinostat (D) in Hep3B cells. Gene expression was normalized to β-actin and expressed relative to untreated controls (set at 1.0). Asterisks indicate statistically significant differences in gene expression vs. the untreated controls (p<0.01). The symbol (x) indicates that very few viable cells remained after 72 h of treatment in these cells.

Article Snippet: The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).

Techniques: Gene Expression, In Vitro, Quantitative RT-PCR

Journal: International journal of oncology

Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.

doi: 10.3892/ijo.2015.3087

Figure Lengend Snippet: Figure 2. Western blot analysis of expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF), fms-like tyrosine kinase-1 (FLT-1), kinase insert domain containing receptor (KDR), MAPK, p-MAPK in vitro and densitometric quantification. HepG2 and Hep3B cells were incubated with 0.1 and 0.01 µM panobinostat for 12, 24 and 48 h. Western blot results show representative examples for expression of CTGF, VEGF, FLT-1, KDR, MAPK and p-MAPK as well as β-actin, which served as loading control (A). Protein expression analyzed using western blot analysis was quantified by densitometry (B). Shown are expression values for CTGF, MAPK, p-MAPK, KDR and VEGF after treatment of HepG2 and Hep3B cell lines with 0.01 and 0.1 µM of panobinostat for 12-48 h.

Article Snippet: The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).

Techniques: Western Blot, Expressing, In Vitro, Incubation, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/β-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12

doi: 10.1016/j.omtn.2021.04.016

Figure Lengend Snippet: PRR34-AS1 expression is elevated in HCC cells (A) UCSC database presented PRR34-AS1 expression profile in multiple human normal tissues, including liver tissues. (B) NONCODE database indicated the profile of PRR34-AS1 expression in different normal tissue samples. (C) GEPIA2 database exhibited PRR34-AS1 expression pattern in 369 cases of LIHC tissues and 160 cases of normal tissues. (D) Quantitative real-time RT-PCR analyzed PRR34-AS1 expression in HCC cell lines (Hep 3B, SK-HEP-1, Huh7, MHCC97-H, and HCCLM3) and human normal hepatocyte cell line (THLE-3). (E and F) Subcellular fractionation and FISH experiments determined PRR34-AS1 location in HCC cells. (G) Knockdown efficiencies of sh-PRR34-AS1#1&2&3 in MHCC97-H and HCCLM3 cells, as well as overexpression efficiency of pcDNA3.1/PRR34-AS1 in Hep 3B cells, were evaluated via quantitative real-time RT-PCR. ∗p < 0.05, ∗∗p < 0.01.

Article Snippet: Human HCC cell lines (Hep 3B and SK-HEP-1), human normal hepatocyte cell line (THLE-3), and human embryonic kidney cell line (HEK293T) were acquired from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Expressing, Quantitative RT-PCR, Fractionation, Knockdown, Over Expression

Journal: Molecular Therapy. Nucleic Acids

Article Title: lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/β-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12

doi: 10.1016/j.omtn.2021.04.016

Figure Lengend Snippet: PRR34-AS1 facilitates HCC cell proliferation in vitro and tumor growth in vivo (A) CCK-8 assays tested the changes in cell proliferation ability induced by PRR34-AS1 silencing in MHCC97-H and HCCLM3 cells and induced by PRR34-AS1 upregulation in Hep 3B cells. (B) Colony formation assays measured the number of colonies formed under PRR34-AS1 silencing in MHCC97-H, HCCLM3 cells, or under PRR34-AS1 upregulation in Hep 3B cells. (C and D) TUNEL assays and flow cytometry analysis assessed the apoptosis rate when PRR34-AS1 was downregulated in HCCLM3 cells (E) Representative pictures of xenografts derived from HCCLM3 cells transfected with sh-NC or sh-PRR34-AS1#1. (F) The grow curves of tumors from two different groups. (G and H) The final tumor volume and weight were measured. ∗p < 0.05, ∗∗p < 0.01.

Article Snippet: Human HCC cell lines (Hep 3B and SK-HEP-1), human normal hepatocyte cell line (THLE-3), and human embryonic kidney cell line (HEK293T) were acquired from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: In Vitro, In Vivo, CCK-8 Assay, TUNEL Assay, Flow Cytometry, Derivative Assay, Transfection

Journal: Molecular Therapy. Nucleic Acids

Article Title: lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/β-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12

doi: 10.1016/j.omtn.2021.04.016

Figure Lengend Snippet: PRR34-AS1 contributes to cell migration, invasion, and EMT process in HCC cells and activates the Wnt/β-catenin pathway (A) Wound healing assays detected the migration ability of indicated HCC cells when PRR34-AS1 was knocked down or upregulated. (B and C) Transwell experiments analyzed the migration and invasion properties in PRR34-AS1 silenced MHCC97-H and HCCLM3 cells, as well as in PRR34-AS1 upregulated Hep 3B cells. (D) Western blot assay examined the protein levels of E-cadherin, N-cadherin, and Vimentin in HCC cells under PRR34-AS1 depletion or overexpression. (E) H&E staining evaluated the metastatic ability of HCCLM3 cells after PRR34-AS1 depletion. (F) TOP Flash/FOP Flash reporter assays assessed the activity of Wnt/β-catenin in HCC cells with PRR34-AS1 depletion or overexpression. (G–I) Western blot evaluated the levels of indicated proteins in HCC cells after PRR34-AS1 depletion or overexpression. ∗p < 0.05.

Article Snippet: Human HCC cell lines (Hep 3B and SK-HEP-1), human normal hepatocyte cell line (THLE-3), and human embryonic kidney cell line (HEK293T) were acquired from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Migration, Western Blot, Over Expression, Staining, Activity Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/β-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12

doi: 10.1016/j.omtn.2021.04.016

Figure Lengend Snippet: PRR34-AS1 sponges miR-296-5p in HCC cells (A) LncBase database was used to predict underlying miRNAs that could combine with PRR34-AS1. (B) RNA pull-down assays assessed the abundance of candidate miRNAs in biotinylated PRR34-AS1 group in Hep 3B cells. (C) ENCORI database predicted the underlying binding sites between PRR34-AS1 and miR-296-5p. (D) Quantitative real-time RT-PCR analyzed miR-296-5p expression pattern in HCC cells (Hep 3B, SK-HEP-1, Huh7, MHCC97-H, and HCCLM3) and human normal hepatocyte cells (THLE-3). (E) RIP assays assessed the abundance of PRR34-AS1 and miR-296-5p in AGO2 complex. (F) Luciferase reporter assays detected the luciferase activity of PRR34-AS1-WT or PRR34-AS1-Mut under miR-296-5p upregulation in HCC cells. ∗p < 0.05, ∗∗p < 0.01.

Article Snippet: Human HCC cell lines (Hep 3B and SK-HEP-1), human normal hepatocyte cell line (THLE-3), and human embryonic kidney cell line (HEK293T) were acquired from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Binding Assay, Quantitative RT-PCR, Expressing, Luciferase, Activity Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/β-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12

doi: 10.1016/j.omtn.2021.04.016

Figure Lengend Snippet: PRR34-AS1 aggravates HCC cell proliferation, migration, and EMT through targeting miR-296-5p (A) Quantitative real-time RT-PCR detected the expression of miR-296-5p in HCCLM3 cells under indicated transfections. (B and C) CCK-8 and colony formation assays examined the proliferation ability of indicated HCCLM3 cells. (D and E) TUNEL and flow cytometry experiments analyzed the apoptosis rate of indicated HCCLM3 cells. (F–H) Wound healing and Transwell assays detected the migratory and invasive capacities of indicated HCCLM3 cells. (I) Western blot examined the protein levels of E-cadherin, N-cadherin, and Vimentin in HCCLM3 cells under different conditions. ∗p < 0.05.

Article Snippet: Human HCC cell lines (Hep 3B and SK-HEP-1), human normal hepatocyte cell line (THLE-3), and human embryonic kidney cell line (HEK293T) were acquired from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Migration, Quantitative RT-PCR, Expressing, Transfection, CCK-8 Assay, TUNEL Assay, Flow Cytometry, Western Blot

Journal: Molecular Therapy. Nucleic Acids

Article Title: lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/β-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12

doi: 10.1016/j.omtn.2021.04.016

Figure Lengend Snippet: E2F2 and SOX12 are identified as the targets of miR-296-5p in HCC cells (A) The mirDIP, microT, PITA, and miRmap databases were used to screen underlying mRNAs that potentially combined with miR-296-5p. (B) Quantitative real-time RT-PCR analyzed the expression of candidate targets (ZNF76, HMGA1, FAM53B, FGFR3, E2F2, HIPK1, SOX12, CDK16, BMF, and SLC16A3) in PRR34-AS1 silenced HCCLM3 cells. (C) ENCORI predicted the binding sites between E2F2/SOX12 and miR-296-5p. (D) Quantitative real-time RT-PCR detected E2F2 and SOX12 mRNA levels in HCC cells (Hep 3B, SK-HEP-1, Huh7, MHCC97-H, and HCCLM3) and THLE-3 cells. (E) Western blot assay analyzed the protein levels of E2F2 and SOX12 in PRR34-AS1 silenced or overexpressed HCC cells. (F) RIP assays assessed the enrichments of PRR34-AS1, miR-296-5p, and E2F2/SOX12 in anti-AGO2 complex. (G) Luciferase reporter experiments assessed the luciferase activity of E2F2-3′ UTR-WT/Mut and SOX12-WT/Mut in HEK293T cells with different transfections. ∗p < 0.05, ∗∗p < 0.01.

Article Snippet: Human HCC cell lines (Hep 3B and SK-HEP-1), human normal hepatocyte cell line (THLE-3), and human embryonic kidney cell line (HEK293T) were acquired from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Quantitative RT-PCR, Expressing, Binding Assay, Western Blot, Luciferase, Activity Assay, Transfection

Journal: Molecular Therapy. Nucleic Acids

Article Title: lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/β-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12

doi: 10.1016/j.omtn.2021.04.016

Figure Lengend Snippet: E2F2 activates PRR34-AS1 transcription in HCC cells (A) Western blot analyzed the knockdown or overexpression efficiencies of E2F2 in HCC cells. (B and C) The levels of E2F2 and PRR34-AS1 in indicated HCC cells were examined via quantitative real-time RT-PCR. (D) ChIP experiments measured the connection between PRR34-AS1 promoter and E2F2 in HCC cells. (E) The binding motif of E2F2 were predicted by JASPAR. (F) Luciferase reporter experiments assessed the luciferase activities of PRR34-AS1-Pro-WT and PRR34-AS1-Pro-Mut in HCC cells after E2F2 expression was increased or silenced. ∗∗p < 0.01.

Article Snippet: Human HCC cell lines (Hep 3B and SK-HEP-1), human normal hepatocyte cell line (THLE-3), and human embryonic kidney cell line (HEK293T) were acquired from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Western Blot, Knockdown, Over Expression, Quantitative RT-PCR, Binding Assay, Luciferase, Expressing

Journal: Disease markers

Article Title: hsa_circ_0129047 Upregulates LYVE1 to Inhibit Hepatocellular Carcinoma Progression by Sponging miR-492.

doi: 10.1155/2023/6978234

Figure Lengend Snippet: FIGURE 2: circ_0129047 overexpression delays in vitro and in vivo HCC growth. Overexpression of circ_0129047 (OE-circ) and empty vectors (OE-NC) was induced in Hep 3B and Huh7 cells. (a) RT-qPCR was verifying the exogenous expression of circ_0129047 in Hep 3B and Huh7 cells. (b) CCK8 assays examining the proliferation of Hep 3B and Huh7 cells transfected with OE-circ and OE-NC. (c) Scratch migration assay for examining HCC cell migration. (d) HCC cell invasion ability was detected using a transwell invasion assay. (e) Hep 3B cells overexpressing circ_0129047 or NC were introduced into nude mice through subcutaneous flank injection. Tumor volumes were recorded every 7 days, and xenograft tumors were excised and weighed at 5 weeks. The xenograft tumors were photographed, measured, and weighed. ∗∗P<0:001, vs. OE-NC.

Article Snippet: A human liver cell line (THLE2) and two HCC cell lines (Hep 3B and SNU-182) were purchased from the American Type Culture Collection (ATCC), Manassas, VA, USA.

Techniques: Over Expression, In Vitro, In Vivo, Quantitative RT-PCR, Expressing, Transfection, Migration, Transwell Invasion Assay, Injection

Journal: Disease markers

Article Title: hsa_circ_0129047 Upregulates LYVE1 to Inhibit Hepatocellular Carcinoma Progression by Sponging miR-492.

doi: 10.1155/2023/6978234

Figure Lengend Snippet: FIGURE 4: miR-492 downregulation is critical for the inhibitory effect of circ_0129047 on HCC cell survival. Hep 3B and Huh7 cells were transfected with OE-NC, OE-circ (OE-circ_0129047), miR-492 mimic, NC mimic, or OE-circ+mimic. (a) CCK8 assays were conducted to determine HCC cell proliferation. (b) Scratch migration assays were conducted to evaluate the migration rate of HCC cells after 24 hr of transfection. (c) Transwell migration assays were conducted to examine HCC cell invasion after 48 hr of transfection. ∗P<0:05; ∗∗P<0:001, vs. mimic; ##P<0:001, vs.mimic-NC; &P<0:05; &&P<0:001, vs.OE + mimic.

Article Snippet: A human liver cell line (THLE2) and two HCC cell lines (Hep 3B and SNU-182) were purchased from the American Type Culture Collection (ATCC), Manassas, VA, USA.

Techniques: Transfection, Migration

Journal: Disease markers

Article Title: hsa_circ_0129047 Upregulates LYVE1 to Inhibit Hepatocellular Carcinoma Progression by Sponging miR-492.

doi: 10.1155/2023/6978234

Figure Lengend Snippet: FIGURE 5: MiR-492 targets LYVE1. (a) TargetScan was used to identify the target of miR-492. (b) Luciferase activity driven by 3′UTR LYVE1 MUT and WT was assessed in Hep 3B and Huh7 cells cotransfected with miR-492 mimic or mimic NC. ∗∗P<0:001, vs. miR-NC. (c) RT- qPCR analysis of LYVE1 expression in HCC and normal tissues. (d) RT-qPCR analysis of LYVE1 in THLE2 and HCC cells. ∗∗P<0:001, vs. THLE2. (e) Pearson analysis of the association between LYVE1 and miR-492 in HCC tissues. (f) Western blotting was conducted to examine the LYVE1 expression in Hep 3B and Huh7 cells transfected with OE-NC, mimic NC, OE-circ mimic, or OE-circ + mimic. ∗∗P<0:001, vs. OE-NC; ##P<0:001, vs.mimic-NC; &&P<0:001, vs.OE- circ + mimic.

Article Snippet: A human liver cell line (THLE2) and two HCC cell lines (Hep 3B and SNU-182) were purchased from the American Type Culture Collection (ATCC), Manassas, VA, USA.

Techniques: Luciferase, Activity Assay, Quantitative RT-PCR, Expressing, Western Blot, Transfection

Journal: Disease markers

Article Title: hsa_circ_0129047 Upregulates LYVE1 to Inhibit Hepatocellular Carcinoma Progression by Sponging miR-492.

doi: 10.1155/2023/6978234

Figure Lengend Snippet: FIGURE 6: LYVE1 downregulation contributes to the oncogenic behaviors of miR-492. Hep 3B and Huh7 cells were transfected with OE-NC, mimic NC, OE-LYVE1 mimic, or OE-LYVE1+mimic. (a) Western blot conducted to examine LYVE1 expression in Hep 3B and Huh7 cells. (b) The CCK8 assay was conducted to determine HCC cell proliferation. (c) Scratch migration assays were conducted to evaluate the migration rate of HCC cells after 24 hr of transfection. (d) Transwell migration assays were conducted to examine HCC cell invasion after 48 hr of transfection. ∗∗P<0:001, vs.OE-NC; #P<0:05; ##P<0:001, vs. mimic-NC; &P<0:05; &&P<0:001, vs. OE + mimic.

Article Snippet: A human liver cell line (THLE2) and two HCC cell lines (Hep 3B and SNU-182) were purchased from the American Type Culture Collection (ATCC), Manassas, VA, USA.

Techniques: Transfection, Western Blot, Expressing, CCK-8 Assay, Migration

Journal: PLoS ONE

Article Title: Combined Therapy with Cytokine-Induced Killer Cells and Oncolytic Adenovirus Expressing IL-12 Induce Enhanced Antitumor Activity in Liver Tumor Model

doi: 10.1371/journal.pone.0044802

Figure Lengend Snippet: ( A ) Schematic description of the structures of AdCN103, AdCN205-GFP and AdCN205-IL12. In AdCN103, the E1A promoter was replaced by hTERT promoter and deletion of the adenoviral genome 923 to 946 nucleotides, which enables viral replication within malignant cells with abnormal RB functions. In AdCN205-GFP and AdCN205-IL12, E3 6.7 K/gp19K genes were substituted by GFP reporter gene and hIL-12 therapeutic gene, respectively. ( B ) Expression of transgene in the cells after infection with oncolytic adenoviruses. Tumor cells (HuH-7) and normal cells (AKN-1) were infected with AdCN205-IL12 at the multiplicity of infection (MOI) of 10. At different time points, the culture supernatant was collected for determination of hIL-12 levels by ELISA. ( C ) hIL-12 level in the cells infected with Ad-IL12 at the MOI of 10. The data was presented as the mean ± SD of three independent experiments. ( D ) Representative photomicrographs were obtained from BEL7404 and AKN-1 infected with AdCN205-EGFP at the MOI of 10. Original magnification, 200×. ( E ) Selective replication of oncolytic adenoviral vectors in vitro . Tumor cells (BEL7404, SMMC7721, MHCC-97H, HuH-7, Hep3B) and normal cells (AKN-1) were infected with AdCN205-GFP, AdCN205-IL12 or Ad-IL12 at the MOI of 10 respectively. At 48 hours after viral infection, cells and medium were harvested, and viral particles were released by three cycles of freezing and thawing. The viral titers were measured by using plaque assay of QuickTiter™ Adenovirus Titer Immunoassay Kit on HEK293 cells. The data was presented as the mean ± SD of three independent experiments.

Article Snippet: Human hepatocellular carcinoma (HCC) cell lines Hep3B (HBs pos , undetected Rb), were purchased from American Tissue Culture Collection (ATCC, Manassas, VA, USA), BEL7404 (HBs neg , Rb wt ), SMMC7721 (HBs neg , Rb wt ), MHCC97H (HBs pos , Rb wt hyperphosphorylated) and HuH-7 (HBs neg , Rb wt hyperphosphorylated) , , were purchased from the Shanghai Cell Collection, China.

Techniques: Expressing, Infection, Enzyme-linked Immunosorbent Assay, In Vitro, Plaque Assay

Journal: PLoS ONE

Article Title: Combined Therapy with Cytokine-Induced Killer Cells and Oncolytic Adenovirus Expressing IL-12 Induce Enhanced Antitumor Activity in Liver Tumor Model

doi: 10.1371/journal.pone.0044802

Figure Lengend Snippet: Liver tumor cells (BEL7404, Hep3B and HuH-7) and normal cells (AKN-1) were infected with AdCN205-GFP, AdCN205-IL12 or Ad-IL12, at the MOI of 10. At different time points after infection, the cell survival was measured by CCK8 assay. Results were expressed as percentage of untreated control. The data was presented as the mean ± SD of three independent experiments. p = 0.035357 (AdCN205-GFP) and 0.033118 (AdCN205-IL12) compared with Ad-IL12 in figure A; P = 0.02159 (AdCN205-GFP) and 0.042144 (AdCN205-IL12) compared with Ad-IL12 in figure B; P = 0.045401 (AdCN205-GFP) and 0.048508 (AdCN205-IL12) compared with Ad-IL12 in figure C.

Article Snippet: Human hepatocellular carcinoma (HCC) cell lines Hep3B (HBs pos , undetected Rb), were purchased from American Tissue Culture Collection (ATCC, Manassas, VA, USA), BEL7404 (HBs neg , Rb wt ), SMMC7721 (HBs neg , Rb wt ), MHCC97H (HBs pos , Rb wt hyperphosphorylated) and HuH-7 (HBs neg , Rb wt hyperphosphorylated) , , were purchased from the Shanghai Cell Collection, China.

Techniques: Infection, CCK-8 Assay, Control

Journal: PLoS ONE

Article Title: Combined Therapy with Cytokine-Induced Killer Cells and Oncolytic Adenovirus Expressing IL-12 Induce Enhanced Antitumor Activity in Liver Tumor Model

doi: 10.1371/journal.pone.0044802

Figure Lengend Snippet: Liver tumor cells (HuH-7 and Hep3B) were treated with CIK cells alone at effector:target ratio of 10∶1, or AdCN205-GFP, AdCN205-IL12 at the MOI of 10, or treated with both CIK at effector:target ratio of 10∶1 and AdCN205-GFP or AdCN205-IL12 at the MOI of 10. The cell survival was determined by measuring luciferase activity. Results were expressed as percentage of untreated control. The data was presented as the mean ± SD of three independent experiments.

Article Snippet: Human hepatocellular carcinoma (HCC) cell lines Hep3B (HBs pos , undetected Rb), were purchased from American Tissue Culture Collection (ATCC, Manassas, VA, USA), BEL7404 (HBs neg , Rb wt ), SMMC7721 (HBs neg , Rb wt ), MHCC97H (HBs pos , Rb wt hyperphosphorylated) and HuH-7 (HBs neg , Rb wt hyperphosphorylated) , , were purchased from the Shanghai Cell Collection, China.

Techniques: Luciferase, Activity Assay, Control