human hepatocellular carcinoma cell lines huh7  (ATCC)


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    ATCC human hepatocellular carcinoma cell lines huh7
    PI3K/AKT/NRF2 pathway activation is required for sorafenib-induced ABCC5 expression. (A) Western blot analysis demonstrated the expression of PI3K, p-PI3K, AKT, and p-AKT in <t>HuH7</t> and Sk-Hep-1 cells treated with sorafenib (3 μM) for 24 h. (B) HuH7 cells were treated with sorafenib (3 μM) for 24 h, and the protein expression of p-PI3K, p-AKT, NRF2 and ABCC5 were detected by Western blot assays after drug withdrawal. (C) HuH7 cells were treated with SC79 (5 μg/ml), SB216763 (10 μM) and LY294002 (10 μM) for 24 h, and the protein expression of p-AKT, NRF2 and ABCC5 were determined by Western blot assays. (D) Western blot analysis examined the protein expression of PI3K, p-PI3K, AKT, and p-AKT in HuH7-SR cells. (E) HuH7-SR cells were treated with LY294002 (10 μM) for 24 h, and the expression of p-AKT, NRF2 and ABCC5 were detected by Western blot assays. (F) HuH7-SR cells were treated with LY294002 (10 μM) for 24 h, and the subcellular localization of NRF2 in indicated cells was assessed by confocal microscopy (original magnification, × 400). Scale bars, 50 μm. (G, H) After transfection with siRNA, the protein expression of NRF2 in Sk-Hep-1 cells was determined by qRT-PCR and Western blot assays. (I) NRF2 expression was down-regulated by siRNA, ML385 (5 μM) and Brusatol (50 nM) in Sk-Hep-1 cells. The protein expression of NRF2 and ABCC5 were determined by Western blot assays. (J) HuH7-SR cells were treated with sorafenib (10 μM) with or without NRF2 inhibitors (Brusatol, 50nM; MK571, 10 µM). Western blot analysis detected the protein expression of NRF2 and ABCC5. (K) After treatment with LY294002 (10 μM), ML385 (5 μM) and brusatol (50 nM) for 24 h, the cell activity of Sk-Hep-1 cells was evaluated by CCK-8 assays. (L) IHC staining detected the expression of p-PI3K, NRF2 and ABCC5 in tumor tissue formed by HuH7 cells and HuH7-SR cells. Representative figures were shown. Scale bars, 50 μm. * p
    Human Hepatocellular Carcinoma Cell Lines Huh7, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human hepatocellular carcinoma cell lines huh7/product/ATCC
    Average 86 stars, based on 8 article reviews
    Price from $9.99 to $1999.99
    human hepatocellular carcinoma cell lines huh7 - by Bioz Stars, 2022-11
    86/100 stars

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    1) Product Images from "ABCC5 facilitates the acquired resistance of sorafenib through the inhibition of SLC7A11-induced ferroptosis in hepatocellular carcinoma"

    Article Title: ABCC5 facilitates the acquired resistance of sorafenib through the inhibition of SLC7A11-induced ferroptosis in hepatocellular carcinoma

    Journal: Neoplasia (New York, N.Y.)

    doi: 10.1016/j.neo.2021.11.002

    PI3K/AKT/NRF2 pathway activation is required for sorafenib-induced ABCC5 expression. (A) Western blot analysis demonstrated the expression of PI3K, p-PI3K, AKT, and p-AKT in HuH7 and Sk-Hep-1 cells treated with sorafenib (3 μM) for 24 h. (B) HuH7 cells were treated with sorafenib (3 μM) for 24 h, and the protein expression of p-PI3K, p-AKT, NRF2 and ABCC5 were detected by Western blot assays after drug withdrawal. (C) HuH7 cells were treated with SC79 (5 μg/ml), SB216763 (10 μM) and LY294002 (10 μM) for 24 h, and the protein expression of p-AKT, NRF2 and ABCC5 were determined by Western blot assays. (D) Western blot analysis examined the protein expression of PI3K, p-PI3K, AKT, and p-AKT in HuH7-SR cells. (E) HuH7-SR cells were treated with LY294002 (10 μM) for 24 h, and the expression of p-AKT, NRF2 and ABCC5 were detected by Western blot assays. (F) HuH7-SR cells were treated with LY294002 (10 μM) for 24 h, and the subcellular localization of NRF2 in indicated cells was assessed by confocal microscopy (original magnification, × 400). Scale bars, 50 μm. (G, H) After transfection with siRNA, the protein expression of NRF2 in Sk-Hep-1 cells was determined by qRT-PCR and Western blot assays. (I) NRF2 expression was down-regulated by siRNA, ML385 (5 μM) and Brusatol (50 nM) in Sk-Hep-1 cells. The protein expression of NRF2 and ABCC5 were determined by Western blot assays. (J) HuH7-SR cells were treated with sorafenib (10 μM) with or without NRF2 inhibitors (Brusatol, 50nM; MK571, 10 µM). Western blot analysis detected the protein expression of NRF2 and ABCC5. (K) After treatment with LY294002 (10 μM), ML385 (5 μM) and brusatol (50 nM) for 24 h, the cell activity of Sk-Hep-1 cells was evaluated by CCK-8 assays. (L) IHC staining detected the expression of p-PI3K, NRF2 and ABCC5 in tumor tissue formed by HuH7 cells and HuH7-SR cells. Representative figures were shown. Scale bars, 50 μm. * p
    Figure Legend Snippet: PI3K/AKT/NRF2 pathway activation is required for sorafenib-induced ABCC5 expression. (A) Western blot analysis demonstrated the expression of PI3K, p-PI3K, AKT, and p-AKT in HuH7 and Sk-Hep-1 cells treated with sorafenib (3 μM) for 24 h. (B) HuH7 cells were treated with sorafenib (3 μM) for 24 h, and the protein expression of p-PI3K, p-AKT, NRF2 and ABCC5 were detected by Western blot assays after drug withdrawal. (C) HuH7 cells were treated with SC79 (5 μg/ml), SB216763 (10 μM) and LY294002 (10 μM) for 24 h, and the protein expression of p-AKT, NRF2 and ABCC5 were determined by Western blot assays. (D) Western blot analysis examined the protein expression of PI3K, p-PI3K, AKT, and p-AKT in HuH7-SR cells. (E) HuH7-SR cells were treated with LY294002 (10 μM) for 24 h, and the expression of p-AKT, NRF2 and ABCC5 were detected by Western blot assays. (F) HuH7-SR cells were treated with LY294002 (10 μM) for 24 h, and the subcellular localization of NRF2 in indicated cells was assessed by confocal microscopy (original magnification, × 400). Scale bars, 50 μm. (G, H) After transfection with siRNA, the protein expression of NRF2 in Sk-Hep-1 cells was determined by qRT-PCR and Western blot assays. (I) NRF2 expression was down-regulated by siRNA, ML385 (5 μM) and Brusatol (50 nM) in Sk-Hep-1 cells. The protein expression of NRF2 and ABCC5 were determined by Western blot assays. (J) HuH7-SR cells were treated with sorafenib (10 μM) with or without NRF2 inhibitors (Brusatol, 50nM; MK571, 10 µM). Western blot analysis detected the protein expression of NRF2 and ABCC5. (K) After treatment with LY294002 (10 μM), ML385 (5 μM) and brusatol (50 nM) for 24 h, the cell activity of Sk-Hep-1 cells was evaluated by CCK-8 assays. (L) IHC staining detected the expression of p-PI3K, NRF2 and ABCC5 in tumor tissue formed by HuH7 cells and HuH7-SR cells. Representative figures were shown. Scale bars, 50 μm. * p

    Techniques Used: Activation Assay, Expressing, Western Blot, Confocal Microscopy, Transfection, Quantitative RT-PCR, Activity Assay, CCK-8 Assay, Immunohistochemistry, Staining

    Sorafenib induces ABCC5 expression in human HCC cells. (A) Data from GSE96793 showed that the expression of ABCC members were markedly increased in sorafenib-resistant cells compared with untreated cells. (B) HuH7 cells were treated with sorafenib (3 µM) for 24 h, and the mRNA expression levels of ABCC members were examined by qRT-PCR ( n = 3, * P
    Figure Legend Snippet: Sorafenib induces ABCC5 expression in human HCC cells. (A) Data from GSE96793 showed that the expression of ABCC members were markedly increased in sorafenib-resistant cells compared with untreated cells. (B) HuH7 cells were treated with sorafenib (3 µM) for 24 h, and the mRNA expression levels of ABCC members were examined by qRT-PCR ( n = 3, * P

    Techniques Used: Expressing, Quantitative RT-PCR

    ABCC5 mediates the acquired resistance to sorafenib in vitro. (A, B) qRT-PCR and Western blot analysis detected the expression of ABCC5 in HCC cells after knockdown and overexpression of ABCC5. (C) HuH7 cells were transfected with LV-ABCC5 and were treated with 3 μM sorafenib for 24 h. UPLC8-MS/MS was used to examine the intercellular concentration of sorafenib. The formation rates of M3, 4, 5 were expressed as relative ratios (Mean ± SD). (D) HuH7-SR cells were treated with 3 μM sorafenib for 24 h, and the intercellular concentration of sorafenib was determined by UPLC8-MS/MS. The formation rates of M3, 4, 5 were expressed as relative ratios (Mean ± SD). (E) The effect of the ABCC inhibitor MK571 (10 μM) on sorafenib resistance was evaluated in HuH7 and Sk-Hep-1 cells by CCK-8 assays. (F) qRT-PCR and Western blot analysis detected the expression of ABCC5 in HuH7 cells and ABCC5-knockdown HuH7-SR cells. (G) Clonogenic cell survival assay. HuH7-SR cells were treated with sorafenib (10 µM) for 24 h, then 1000 cells were plated into 6-well plates. Colonies were visualized by crystal violet staining two weeks later. # P > 0.05, * P
    Figure Legend Snippet: ABCC5 mediates the acquired resistance to sorafenib in vitro. (A, B) qRT-PCR and Western blot analysis detected the expression of ABCC5 in HCC cells after knockdown and overexpression of ABCC5. (C) HuH7 cells were transfected with LV-ABCC5 and were treated with 3 μM sorafenib for 24 h. UPLC8-MS/MS was used to examine the intercellular concentration of sorafenib. The formation rates of M3, 4, 5 were expressed as relative ratios (Mean ± SD). (D) HuH7-SR cells were treated with 3 μM sorafenib for 24 h, and the intercellular concentration of sorafenib was determined by UPLC8-MS/MS. The formation rates of M3, 4, 5 were expressed as relative ratios (Mean ± SD). (E) The effect of the ABCC inhibitor MK571 (10 μM) on sorafenib resistance was evaluated in HuH7 and Sk-Hep-1 cells by CCK-8 assays. (F) qRT-PCR and Western blot analysis detected the expression of ABCC5 in HuH7 cells and ABCC5-knockdown HuH7-SR cells. (G) Clonogenic cell survival assay. HuH7-SR cells were treated with sorafenib (10 µM) for 24 h, then 1000 cells were plated into 6-well plates. Colonies were visualized by crystal violet staining two weeks later. # P > 0.05, * P

    Techniques Used: In Vitro, Quantitative RT-PCR, Western Blot, Expressing, Over Expression, Transfection, Tandem Mass Spectroscopy, Concentration Assay, CCK-8 Assay, Clonogenic Cell Survival Assay, Staining

    ABCC5 negatively regulates ferroptosis by stabilizing SLC7A11. (A) Western blot analysis determined the expression of SLC7A11 in HuH7-SR cells. (B,C) Western blot analysis detected the expression of ABCC5 and SLC7A11 in HuH7-SR cells after knockdown and overexpression of ABCC5. (D,E) HuH7-SR cells were treated with ML385 (5 μM), brusatol (50 nM),MK571 (10 μM), Erastin (10 μM) and RSL3 (3 μM) for 24 h, and the protein expression of ABCC5 and SLC7A11 in HuH7-SR cell lines were determined by qRT-PCR and Western blot assays. (F) The ABCC5-knockdown HuH7-SR cells were treated with sorafenib (10 µM) with or without Erastin(10 μM) for 24 h, and the levels of glutathione (GSH) and lipid ROS were assayed ( n = 3, * P
    Figure Legend Snippet: ABCC5 negatively regulates ferroptosis by stabilizing SLC7A11. (A) Western blot analysis determined the expression of SLC7A11 in HuH7-SR cells. (B,C) Western blot analysis detected the expression of ABCC5 and SLC7A11 in HuH7-SR cells after knockdown and overexpression of ABCC5. (D,E) HuH7-SR cells were treated with ML385 (5 μM), brusatol (50 nM),MK571 (10 μM), Erastin (10 μM) and RSL3 (3 μM) for 24 h, and the protein expression of ABCC5 and SLC7A11 in HuH7-SR cell lines were determined by qRT-PCR and Western blot assays. (F) The ABCC5-knockdown HuH7-SR cells were treated with sorafenib (10 µM) with or without Erastin(10 μM) for 24 h, and the levels of glutathione (GSH) and lipid ROS were assayed ( n = 3, * P

    Techniques Used: Western Blot, Expressing, Over Expression, Quantitative RT-PCR

    Knocking down targeted ABCC5 enhances the anticancer activity of sorafenib in the resistant HCC cells in vivo. (A) Nude mice were injected subcutaneously with HuH7-SR cells (2 × 10 6 cells/mouse) and treated with sorafenib (10 mg/kg/i.p., once every other day) at day seven for two weeks ( n = 7 mice/group). (B) Tumor volume of each mice was calculated every two days. (C) In addition, the tumor weight was measured at day 22 (* P
    Figure Legend Snippet: Knocking down targeted ABCC5 enhances the anticancer activity of sorafenib in the resistant HCC cells in vivo. (A) Nude mice were injected subcutaneously with HuH7-SR cells (2 × 10 6 cells/mouse) and treated with sorafenib (10 mg/kg/i.p., once every other day) at day seven for two weeks ( n = 7 mice/group). (B) Tumor volume of each mice was calculated every two days. (C) In addition, the tumor weight was measured at day 22 (* P

    Techniques Used: Activity Assay, In Vivo, Mouse Assay, Injection

    2) Product Images from "Generation of a tumor- and tissue-specific episomal non-viral vector system"

    Article Title: Generation of a tumor- and tissue-specific episomal non-viral vector system

    Journal: BMC Biotechnology

    doi: 10.1186/1472-6750-13-49

    Influence of the hCMV enhancer on liver promoter mediated transfection in hepatocellular carcinoma cells. 50,000 HUH7 cells seeded in 24-well plates were transfected with HD-O polyplexes containing the indicated plasmid (1.5 μg plasmid/well) and the luciferase activity per 10,000 cells determined at indicated time points; n = 2. Open symbols: CMV promoter; gray symbols: liver promoter; full symbols: liver promoter plus hCMV enhancer.
    Figure Legend Snippet: Influence of the hCMV enhancer on liver promoter mediated transfection in hepatocellular carcinoma cells. 50,000 HUH7 cells seeded in 24-well plates were transfected with HD-O polyplexes containing the indicated plasmid (1.5 μg plasmid/well) and the luciferase activity per 10,000 cells determined at indicated time points; n = 2. Open symbols: CMV promoter; gray symbols: liver promoter; full symbols: liver promoter plus hCMV enhancer.

    Techniques Used: Transfection, Plasmid Preparation, Luciferase, Activity Assay

    Hepatoma specific transgene expression with pEPito-hCMV/AFP-oFLuc in vivo. NMRI nu/nu mice bearing subcutaneous HUH7 human hepatoma tumors were injected intravenously with LPEI polyplexes (N/P 6) formed either with pEPito-hCMV/AFP-oFLuc or pEPito-CMV-oFLuc at a dose of 2.5 mg/kg (n = 6 per group). Luciferase activity (RLU/mg tissue) is shown in lysates of lung, tumor and liver 24 h after transfection; grey bars: pEPito-CMV-oFLuc, full bars: pEPito-hCMV/AFP-oFLuc; n = 6; * p
    Figure Legend Snippet: Hepatoma specific transgene expression with pEPito-hCMV/AFP-oFLuc in vivo. NMRI nu/nu mice bearing subcutaneous HUH7 human hepatoma tumors were injected intravenously with LPEI polyplexes (N/P 6) formed either with pEPito-hCMV/AFP-oFLuc or pEPito-CMV-oFLuc at a dose of 2.5 mg/kg (n = 6 per group). Luciferase activity (RLU/mg tissue) is shown in lysates of lung, tumor and liver 24 h after transfection; grey bars: pEPito-CMV-oFLuc, full bars: pEPito-hCMV/AFP-oFLuc; n = 6; * p

    Techniques Used: Expressing, In Vivo, Mouse Assay, Injection, Luciferase, Activity Assay, Transfection

    3) Product Images from "Efficient Colonization and Therapy of Human Hepatocellular Carcinoma (HCC) Using the Oncolytic Vaccinia Virus Strain GLV-1h68"

    Article Title: Efficient Colonization and Therapy of Human Hepatocellular Carcinoma (HCC) Using the Oncolytic Vaccinia Virus Strain GLV-1h68

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0022069

    Replication efficiency of vaccinia virus strain GLV-1h68 in HuH7 (A) and PLC (B) cells at an MOI of 0.1. Supernatants were collected from virus-infected cells at various time points (hours) post-infection (hpi). Viral titers were determined as pfu per well in triplicates. Averages plus standard deviation are plotted.
    Figure Legend Snippet: Replication efficiency of vaccinia virus strain GLV-1h68 in HuH7 (A) and PLC (B) cells at an MOI of 0.1. Supernatants were collected from virus-infected cells at various time points (hours) post-infection (hpi). Viral titers were determined as pfu per well in triplicates. Averages plus standard deviation are plotted.

    Techniques Used: Planar Chromatography, Infection, Standard Deviation

    Immunohistochemical staining of MHC class II-positive cells in GLV-1h68-infected and uninfected HuH7 or PLC xenograft tumors at 10 dpi. Mice bearing tumors of HuH7 (A, B) or PLC (C, D) origin either were mock treated (A, C) or infected with GLV-1h68 (B, D). Tumor sections were labeled with an anti-MHCII antibody (red) and viral infection was indicated by GFP fluorescence (green). In addition, overlays of MHCII and GFP signals and transmission images (bright-field) are shown. Scale bars represent 1 mm.
    Figure Legend Snippet: Immunohistochemical staining of MHC class II-positive cells in GLV-1h68-infected and uninfected HuH7 or PLC xenograft tumors at 10 dpi. Mice bearing tumors of HuH7 (A, B) or PLC (C, D) origin either were mock treated (A, C) or infected with GLV-1h68 (B, D). Tumor sections were labeled with an anti-MHCII antibody (red) and viral infection was indicated by GFP fluorescence (green). In addition, overlays of MHCII and GFP signals and transmission images (bright-field) are shown. Scale bars represent 1 mm.

    Techniques Used: Immunohistochemistry, Staining, Infection, Planar Chromatography, Mouse Assay, Labeling, Fluorescence, Transmission Assay

    Analysis of GLV-1h68 virus-induced changes in HuH7- or PLC-tumor vascularization by confocal laser microscopy. Determination of vascular density using CD31 immunohistochemistry in virus- treated and non-treated HuH7 or PLC, tumors (A). The vascular density was measured in CD31-labeled tumor cross-sections (n = 6 per group) and presented as mean values +/− standard deviations. The asterisks (**) indicate a significant difference between experimental groups (** P
    Figure Legend Snippet: Analysis of GLV-1h68 virus-induced changes in HuH7- or PLC-tumor vascularization by confocal laser microscopy. Determination of vascular density using CD31 immunohistochemistry in virus- treated and non-treated HuH7 or PLC, tumors (A). The vascular density was measured in CD31-labeled tumor cross-sections (n = 6 per group) and presented as mean values +/− standard deviations. The asterisks (**) indicate a significant difference between experimental groups (** P

    Techniques Used: Planar Chromatography, Microscopy, Immunohistochemistry, Labeling

    Growth of HuH7 and PLC tumors in GLV-1h68- and mock-treated mice. Groups of HuH7 ( Fig. 5A ) or PLC tumor-bearing nude mice ( Fig. 5B ) were either treated with a single dose of 5×10 6 pfu GLV-1h68 (n = 5) or with PBS (mock control, n = 5). Tumor size was measured twice a week. Two-way analysis of variance (2way ANOVA) with Bonferroni post-test was used for comparison of two corresponding data points between groups. P
    Figure Legend Snippet: Growth of HuH7 and PLC tumors in GLV-1h68- and mock-treated mice. Groups of HuH7 ( Fig. 5A ) or PLC tumor-bearing nude mice ( Fig. 5B ) were either treated with a single dose of 5×10 6 pfu GLV-1h68 (n = 5) or with PBS (mock control, n = 5). Tumor size was measured twice a week. Two-way analysis of variance (2way ANOVA) with Bonferroni post-test was used for comparison of two corresponding data points between groups. P

    Techniques Used: Planar Chromatography, Mouse Assay

    Viability of hepatocellular carcinoma HuH7 (A) and PLC (B) cells after GLV-1h68 infection at MOIs of 0.1 and 1.0, respectively. Viable cells after infection with GLV-1h68 were determined by use of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) (Sigma, Taufkirchen, Germany). Mean values (n = 3) and standard deviations are shown as percentages of respective controls.
    Figure Legend Snippet: Viability of hepatocellular carcinoma HuH7 (A) and PLC (B) cells after GLV-1h68 infection at MOIs of 0.1 and 1.0, respectively. Viable cells after infection with GLV-1h68 were determined by use of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) (Sigma, Taufkirchen, Germany). Mean values (n = 3) and standard deviations are shown as percentages of respective controls.

    Techniques Used: Planar Chromatography, Infection, MTT Assay

    4) Product Images from "Synergistic induction of cell death in liver tumor cells by TRAIL and chemotherapeutic drugs via the BH3-only proteins Bim and Bid"

    Article Title: Synergistic induction of cell death in liver tumor cells by TRAIL and chemotherapeutic drugs via the BH3-only proteins Bim and Bid

    Journal: Cell Death & Disease

    doi: 10.1038/cddis.2010.66

    Synergistic induction of cell death by doxorubicin and TRAIL. ( a ) HepG2, Huh7, Hep3B and IHH cells were pretreated by either medium control, 10 ng/ml TRAIL (left panels) or 1 μ g/ml doxorubicin (Dox, right panels), before the exposure to increasing concentration of doxorubicin (left panels) or TRAIL (right panels). Cell death was measured by MTT assay. Mean values±S.D. of quadruplicates of a typical experiment ( n =3) are shown. ( b ) HepG2 cells were treated with 1 μ g/ml doxorubicin, 10 ng/ml TRAIL or the combination thereof for 6 h, and DEVDase activity in cell lysates was measured. Mean values±S.D. of quadruplicates were measured. n =3. ( c ) HepG2 cells were pretreated with medium control or 10 ng/ml TRAIL, and then exposed to increasing doses of doxorubicin. Apoptosis was measured by Annexin V binding. n =2
    Figure Legend Snippet: Synergistic induction of cell death by doxorubicin and TRAIL. ( a ) HepG2, Huh7, Hep3B and IHH cells were pretreated by either medium control, 10 ng/ml TRAIL (left panels) or 1 μ g/ml doxorubicin (Dox, right panels), before the exposure to increasing concentration of doxorubicin (left panels) or TRAIL (right panels). Cell death was measured by MTT assay. Mean values±S.D. of quadruplicates of a typical experiment ( n =3) are shown. ( b ) HepG2 cells were treated with 1 μ g/ml doxorubicin, 10 ng/ml TRAIL or the combination thereof for 6 h, and DEVDase activity in cell lysates was measured. Mean values±S.D. of quadruplicates were measured. n =3. ( c ) HepG2 cells were pretreated with medium control or 10 ng/ml TRAIL, and then exposed to increasing doses of doxorubicin. Apoptosis was measured by Annexin V binding. n =2

    Techniques Used: Concentration Assay, MTT Assay, Activity Assay, Binding Assay

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  • 96
    ATCC hcc cell lines
    Interference of EFNA4 suppressed <t>Huh7</t> <t>cell</t> proliferation, migration and invasion Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4-1/2, and (A) the mRNA level and (B) protein expression of EFNA4 were detected using qRT-PCR and western blot, respectively. (C) CCK-8 assay and (D) colony formation assay were conducted to evaluate cell proliferation ability. (E) Wound-healing assay and (F) Transwell assay were performed to assess cell migration ability and invasion ability, respectively. (G) Western blot was performed to detect protein expression of MMP2 and MMP9. **p
    Hcc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hcc cell lines/product/ATCC
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    hcc cell lines - by Bioz Stars, 2022-11
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    95
    ATCC human liver cancer cell line
    Interference of EFNA4 suppressed <t>Huh7</t> <t>cell</t> proliferation, migration and invasion Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4-1/2, and (A) the mRNA level and (B) protein expression of EFNA4 were detected using qRT-PCR and western blot, respectively. (C) CCK-8 assay and (D) colony formation assay were conducted to evaluate cell proliferation ability. (E) Wound-healing assay and (F) Transwell assay were performed to assess cell migration ability and invasion ability, respectively. (G) Western blot was performed to detect protein expression of MMP2 and MMP9. **p
    Human Liver Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human liver cancer cell line/product/ATCC
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    human liver cancer cell line - by Bioz Stars, 2022-11
    95/100 stars
      Buy from Supplier

    97
    ATCC human hcc cell line huh7
    Interference of EFNA4 suppressed <t>Huh7</t> <t>cell</t> proliferation, migration and invasion Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4-1/2, and (A) the mRNA level and (B) protein expression of EFNA4 were detected using qRT-PCR and western blot, respectively. (C) CCK-8 assay and (D) colony formation assay were conducted to evaluate cell proliferation ability. (E) Wound-healing assay and (F) Transwell assay were performed to assess cell migration ability and invasion ability, respectively. (G) Western blot was performed to detect protein expression of MMP2 and MMP9. **p
    Human Hcc Cell Line Huh7, 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
    https://www.bioz.com/result/human hcc cell line huh7/product/ATCC
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    human hcc cell line huh7 - by Bioz Stars, 2022-11
    97/100 stars
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    Interference of EFNA4 suppressed Huh7 cell proliferation, migration and invasion Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4-1/2, and (A) the mRNA level and (B) protein expression of EFNA4 were detected using qRT-PCR and western blot, respectively. (C) CCK-8 assay and (D) colony formation assay were conducted to evaluate cell proliferation ability. (E) Wound-healing assay and (F) Transwell assay were performed to assess cell migration ability and invasion ability, respectively. (G) Western blot was performed to detect protein expression of MMP2 and MMP9. **p

    Journal: Cancer Biology & Therapy

    Article Title: Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2

    doi: 10.1080/15384047.2022.2149039

    Figure Lengend Snippet: Interference of EFNA4 suppressed Huh7 cell proliferation, migration and invasion Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4-1/2, and (A) the mRNA level and (B) protein expression of EFNA4 were detected using qRT-PCR and western blot, respectively. (C) CCK-8 assay and (D) colony formation assay were conducted to evaluate cell proliferation ability. (E) Wound-healing assay and (F) Transwell assay were performed to assess cell migration ability and invasion ability, respectively. (G) Western blot was performed to detect protein expression of MMP2 and MMP9. **p

    Article Snippet: The immortalized human liver epithelial cell THLE-3, and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3) were purchased from American Type Culture Collection and cultured in DMEM (Gibco; Thermo Fisher Scientific) supplemented with 10% fetal bovine serum (Gibco).

    Techniques: Migration, Transfection, shRNA, Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Colony Assay, Wound Healing Assay, Transwell Assay

    The inhibitory effects of EFNA4 knockdown on Huh7 cell proliferation and invasion were partly abolished by PYGO2 overexpression Huh7 cells were transfected with oe-NC or oe-PYGO2, and the (A) mRNA level and (B) protein expression of PYGO2 were measured. Huh7 cells were transfected with shRNA-EFNA4-2 or co-transfected with shRNA-EFNA4-2 and oe-NC/oe-PYGO2. (C) CCK-8 assay and (D) colony formation assay were conducted to evaluate cell proliferation ability. ***p

    Journal: Cancer Biology & Therapy

    Article Title: Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2

    doi: 10.1080/15384047.2022.2149039

    Figure Lengend Snippet: The inhibitory effects of EFNA4 knockdown on Huh7 cell proliferation and invasion were partly abolished by PYGO2 overexpression Huh7 cells were transfected with oe-NC or oe-PYGO2, and the (A) mRNA level and (B) protein expression of PYGO2 were measured. Huh7 cells were transfected with shRNA-EFNA4-2 or co-transfected with shRNA-EFNA4-2 and oe-NC/oe-PYGO2. (C) CCK-8 assay and (D) colony formation assay were conducted to evaluate cell proliferation ability. ***p

    Article Snippet: The immortalized human liver epithelial cell THLE-3, and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3) were purchased from American Type Culture Collection and cultured in DMEM (Gibco; Thermo Fisher Scientific) supplemented with 10% fetal bovine serum (Gibco).

    Techniques: Over Expression, Transfection, Expressing, shRNA, CCK-8 Assay, Colony Assay

    EFNA4 was positively correlated with PYGO2 in HCC (A–C) From LinkedOimcs database, the EFNA4-associated genes were observed. The correlation between EFNA4 and PYGO2 in HCC was analyzed through (D) LinkedOimcs and (E) GEPIA database. (F) Humanbase website predicted the interaction relationship between EFNA4 and PYGO2. (G) Co-IP verified the interaction between EFNA4 and PYGO2. Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4, and the (H) mRNA level and (i) protein expression of PYGO2 was detected, respectively. **p

    Journal: Cancer Biology & Therapy

    Article Title: Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2

    doi: 10.1080/15384047.2022.2149039

    Figure Lengend Snippet: EFNA4 was positively correlated with PYGO2 in HCC (A–C) From LinkedOimcs database, the EFNA4-associated genes were observed. The correlation between EFNA4 and PYGO2 in HCC was analyzed through (D) LinkedOimcs and (E) GEPIA database. (F) Humanbase website predicted the interaction relationship between EFNA4 and PYGO2. (G) Co-IP verified the interaction between EFNA4 and PYGO2. Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4, and the (H) mRNA level and (i) protein expression of PYGO2 was detected, respectively. **p

    Article Snippet: The immortalized human liver epithelial cell THLE-3, and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3) were purchased from American Type Culture Collection and cultured in DMEM (Gibco; Thermo Fisher Scientific) supplemented with 10% fetal bovine serum (Gibco).

    Techniques: Co-Immunoprecipitation Assay, Transfection, shRNA, Expressing

    The inhibitory effect of EFNA4 knockdown on angiogenesis in Huh7 cells was partly abolished by PYGO2 overexpression Huh7 cells were transfected with shRNA-EFNA4-2 or co-transfected with shRNA-EFNA4-2 and oe-NC/oe-PYGO2, and the tube formation was observed under a light microscopy. (B) The concentration of VEGF and VEGFR2 in the cell supernatant was detected using ELISA assay. **p

    Journal: Cancer Biology & Therapy

    Article Title: Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2

    doi: 10.1080/15384047.2022.2149039

    Figure Lengend Snippet: The inhibitory effect of EFNA4 knockdown on angiogenesis in Huh7 cells was partly abolished by PYGO2 overexpression Huh7 cells were transfected with shRNA-EFNA4-2 or co-transfected with shRNA-EFNA4-2 and oe-NC/oe-PYGO2, and the tube formation was observed under a light microscopy. (B) The concentration of VEGF and VEGFR2 in the cell supernatant was detected using ELISA assay. **p

    Article Snippet: The immortalized human liver epithelial cell THLE-3, and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3) were purchased from American Type Culture Collection and cultured in DMEM (Gibco; Thermo Fisher Scientific) supplemented with 10% fetal bovine serum (Gibco).

    Techniques: Over Expression, Transfection, shRNA, Light Microscopy, Concentration Assay, Enzyme-linked Immunosorbent Assay

    EFNA4 was upregulated in HCC and correlated with poor prognosis GEPIA database were applied to observe the expression level of EFNA4 in tumor samples of HCC patients and normal samples. (B) The correlation between EFNA4 expression and TNM stages in patients. (C) The correlation between EFNA4 expression and overall survival (OS). (D) The correlation between EFNA4 expression and disease free survival (DFS). (e) CCLE database were also employed to evaluate the expression of EFNA4 in different cancer cells. (F) The mRNA level and (G) protein expression of EFNA4 in the immortalized human liver epithelial cell THLE-3 and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3). *p

    Journal: Cancer Biology & Therapy

    Article Title: Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2

    doi: 10.1080/15384047.2022.2149039

    Figure Lengend Snippet: EFNA4 was upregulated in HCC and correlated with poor prognosis GEPIA database were applied to observe the expression level of EFNA4 in tumor samples of HCC patients and normal samples. (B) The correlation between EFNA4 expression and TNM stages in patients. (C) The correlation between EFNA4 expression and overall survival (OS). (D) The correlation between EFNA4 expression and disease free survival (DFS). (e) CCLE database were also employed to evaluate the expression of EFNA4 in different cancer cells. (F) The mRNA level and (G) protein expression of EFNA4 in the immortalized human liver epithelial cell THLE-3 and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3). *p

    Article Snippet: The immortalized human liver epithelial cell THLE-3, and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3) were purchased from American Type Culture Collection and cultured in DMEM (Gibco; Thermo Fisher Scientific) supplemented with 10% fetal bovine serum (Gibco).

    Techniques: Expressing

    Interference of EFNA4 suppressed angiogenesis in Huh7 cells Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4-2, and the tube formation was observed under a light microscopy. The concentration of (B) VEGF and (C) VEGFR2 in the cell supernatant was detected using ELISA assay. **p

    Journal: Cancer Biology & Therapy

    Article Title: Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2

    doi: 10.1080/15384047.2022.2149039

    Figure Lengend Snippet: Interference of EFNA4 suppressed angiogenesis in Huh7 cells Huh7 cells were transfected with shRNA-NC or shRNA-EFNA4-2, and the tube formation was observed under a light microscopy. The concentration of (B) VEGF and (C) VEGFR2 in the cell supernatant was detected using ELISA assay. **p

    Article Snippet: The immortalized human liver epithelial cell THLE-3, and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3) were purchased from American Type Culture Collection and cultured in DMEM (Gibco; Thermo Fisher Scientific) supplemented with 10% fetal bovine serum (Gibco).

    Techniques: Transfection, shRNA, Light Microscopy, Concentration Assay, Enzyme-linked Immunosorbent Assay

    EFNA4/PYGO2 regulated Wnt/β-catenin signaling in Huh7 cells Huh7 cells were transfected with shRNA-EFNA4-2 or co-transfected with shRNA-EFNA4-2 and oe-NC/oe-PYGO2, and the protein expression of β-catenin, cyclin D1, and c-myc was measured by western blot. **p

    Journal: Cancer Biology & Therapy

    Article Title: Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2

    doi: 10.1080/15384047.2022.2149039

    Figure Lengend Snippet: EFNA4/PYGO2 regulated Wnt/β-catenin signaling in Huh7 cells Huh7 cells were transfected with shRNA-EFNA4-2 or co-transfected with shRNA-EFNA4-2 and oe-NC/oe-PYGO2, and the protein expression of β-catenin, cyclin D1, and c-myc was measured by western blot. **p

    Article Snippet: The immortalized human liver epithelial cell THLE-3, and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3) were purchased from American Type Culture Collection and cultured in DMEM (Gibco; Thermo Fisher Scientific) supplemented with 10% fetal bovine serum (Gibco).

    Techniques: Transfection, shRNA, Expressing, Western Blot

    PYGO2 is upregulated in HCC and correlated with poor prognosis (A) GEPIA database were applied to observe the expression level of PYGO2 in tumor samples of HCC patients and normal samples. (B) The correlation between PYGO2 expression and TNM stages in patients. (C) The correlation between PYGO2 expression and overall survival (OS). (D) The correlation between PYGO2 expression and disease free survival (DFS). (E) CCLE database were also employed to evaluate the expression of PYGO2 in different cancer cells. (F) The mRNA level and (G) protein expression of PYGO2 in the immortalized human liver epithelial cell THLE-3 and HCC cell Huh7. *p

    Journal: Cancer Biology & Therapy

    Article Title: Interference of EFNA4 suppresses cell proliferation, invasion and angiogenesis in hepatocellular carcinoma by downregulating PYGO2

    doi: 10.1080/15384047.2022.2149039

    Figure Lengend Snippet: PYGO2 is upregulated in HCC and correlated with poor prognosis (A) GEPIA database were applied to observe the expression level of PYGO2 in tumor samples of HCC patients and normal samples. (B) The correlation between PYGO2 expression and TNM stages in patients. (C) The correlation between PYGO2 expression and overall survival (OS). (D) The correlation between PYGO2 expression and disease free survival (DFS). (E) CCLE database were also employed to evaluate the expression of PYGO2 in different cancer cells. (F) The mRNA level and (G) protein expression of PYGO2 in the immortalized human liver epithelial cell THLE-3 and HCC cell Huh7. *p

    Article Snippet: The immortalized human liver epithelial cell THLE-3, and HCC cell lines (Huh7, MHCC97-H, SNU-449 and HCCLM3) were purchased from American Type Culture Collection and cultured in DMEM (Gibco; Thermo Fisher Scientific) supplemented with 10% fetal bovine serum (Gibco).

    Techniques: Expressing

    LINC01468 destabilizes SHIP2 via ubiquitin proteasome pathway. A , B Western blotting analysis of SHIP2 expression levels in SNU-449 and HCC-LM3 cells after silencing LINC01468 ( A ) or in SNU-182 and Huh7 cells after overexpression of LINC01468 ( B ). C RT-qPCR was used to test the mRNA expression of SHIP2 in indicated cells transfected with (upper panel) or without (lower panel) LINC01468. GAPDH was used for normalization. D , E SNU-182 ( D ) and Huh7 ( E ) transfected with or without LINC01468 were treated with CHX at 20 μg/mL for the indicated times, and the expression of SHIP2 was tested by western blotting. F SNU-182 and Huh7 transfected with or without LINC01468 were treated with MG132 (5 μM for 4 h), and the SHIP2 protein level was tested by western blotting. G Quantification of the results in F. H The LINC01468-overexpressing SNU-182 cells were cotransfected with HA-tagged ubiquitin (HA-Ub) expressed plasmid. After MG132 (5 μM for 4 h) treatment, cell lysates were subjected to western blotting. Anti-HA antibody was used to perform IP. I The cell lysates in H were subjected to Co-IP with the SHIP2 (IP: SHIP2) antibody followed by western blotting. J Western blotting was used to detect cell lysates from Huh7 cells cotransfected with HA-Ub plasmid with or without LINC01468 and treated with MG132 (5 μM for 4 h). K The cell lysates in J were subjected to Co-IP with SHIP2 antibody (IP: SHIP2) followed by western blot analysis. * P

    Journal: Cell Death Discovery

    Article Title: LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2

    doi: 10.1038/s41420-022-01234-8

    Figure Lengend Snippet: LINC01468 destabilizes SHIP2 via ubiquitin proteasome pathway. A , B Western blotting analysis of SHIP2 expression levels in SNU-449 and HCC-LM3 cells after silencing LINC01468 ( A ) or in SNU-182 and Huh7 cells after overexpression of LINC01468 ( B ). C RT-qPCR was used to test the mRNA expression of SHIP2 in indicated cells transfected with (upper panel) or without (lower panel) LINC01468. GAPDH was used for normalization. D , E SNU-182 ( D ) and Huh7 ( E ) transfected with or without LINC01468 were treated with CHX at 20 μg/mL for the indicated times, and the expression of SHIP2 was tested by western blotting. F SNU-182 and Huh7 transfected with or without LINC01468 were treated with MG132 (5 μM for 4 h), and the SHIP2 protein level was tested by western blotting. G Quantification of the results in F. H The LINC01468-overexpressing SNU-182 cells were cotransfected with HA-tagged ubiquitin (HA-Ub) expressed plasmid. After MG132 (5 μM for 4 h) treatment, cell lysates were subjected to western blotting. Anti-HA antibody was used to perform IP. I The cell lysates in H were subjected to Co-IP with the SHIP2 (IP: SHIP2) antibody followed by western blotting. J Western blotting was used to detect cell lysates from Huh7 cells cotransfected with HA-Ub plasmid with or without LINC01468 and treated with MG132 (5 μM for 4 h). K The cell lysates in J were subjected to Co-IP with SHIP2 antibody (IP: SHIP2) followed by western blot analysis. * P

    Article Snippet: Normal human hepatocyte THLE2 and the HCC cell lines (Huh7, SNU-449, SNU-182, and HCC-LM3) were obtained from the American Type Culture Collection (ATCC, USA) (Supplementary Table ).

    Techniques: Western Blot, Expressing, Over Expression, Quantitative RT-PCR, Transfection, Plasmid Preparation, Co-Immunoprecipitation Assay

    m 6 A modification mediated by ALKBH5 upregulates LINC01468. A The enrichment of m 6 A-modified LINC01468 was detected by the RIP-RT-qPCR assay in the indicated cells. B The negative correlation between the levels of LINC01468 and ALKBH5 was confirmed in 26 pairs of NAFLD-HCC patients. C ALKBH5 expression in HCC was analyzed in HCC tissues and corresponding para-cancerous tissues from 26 pairs of NAFLD-HCC patients. D The online website http://m6avar.renlab.org/ was used to predict the m 6 A modification locus of LINC01468 modified by ALKBH5, followed by confirmation by the luciferase reporter assay. E , F Effect of ALKBH5 overexpression in SNU-449 cells ( E ) or knockdown in Huh7 cells ( F ) on LINC01468 expression. G , H Results of RIP-RT-qPCR showing the enrichment of m 6 A-modified LINC01468 following overexpression in SNU-449 cells or silencing in Huh7 cells of ALKBH5. I LINC01468 stability was analyzed in HCC-LM3 cells with ALKBH5 overexpression or silencing in the presence of actinomycin ( D ). The data represent the means ± S.D (* P

    Journal: Cell Death Discovery

    Article Title: LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2

    doi: 10.1038/s41420-022-01234-8

    Figure Lengend Snippet: m 6 A modification mediated by ALKBH5 upregulates LINC01468. A The enrichment of m 6 A-modified LINC01468 was detected by the RIP-RT-qPCR assay in the indicated cells. B The negative correlation between the levels of LINC01468 and ALKBH5 was confirmed in 26 pairs of NAFLD-HCC patients. C ALKBH5 expression in HCC was analyzed in HCC tissues and corresponding para-cancerous tissues from 26 pairs of NAFLD-HCC patients. D The online website http://m6avar.renlab.org/ was used to predict the m 6 A modification locus of LINC01468 modified by ALKBH5, followed by confirmation by the luciferase reporter assay. E , F Effect of ALKBH5 overexpression in SNU-449 cells ( E ) or knockdown in Huh7 cells ( F ) on LINC01468 expression. G , H Results of RIP-RT-qPCR showing the enrichment of m 6 A-modified LINC01468 following overexpression in SNU-449 cells or silencing in Huh7 cells of ALKBH5. I LINC01468 stability was analyzed in HCC-LM3 cells with ALKBH5 overexpression or silencing in the presence of actinomycin ( D ). The data represent the means ± S.D (* P

    Article Snippet: Normal human hepatocyte THLE2 and the HCC cell lines (Huh7, SNU-449, SNU-182, and HCC-LM3) were obtained from the American Type Culture Collection (ATCC, USA) (Supplementary Table ).

    Techniques: Modification, Quantitative RT-PCR, Expressing, Luciferase, Reporter Assay, Over Expression

    Enforced expression of SHIP2 rescues the LINC01468 metabolic phenotypes. A Western blotting analysis of the SHIP2/Akt/mTOR pathway protein in SNU-449 cells cotransfected with or without shLINC01468, together with shSHIP2 or empty vector. B Migration, invasion, ORO staining, and Nile Red staining were performed in SNU-449 cells as described in A . C Western blotting analysis of the SHIP2/Akt/mTOR pathway protein in Huh7 cells cotransfected with LINC01468 or the control, together with SHIP2 or empty vector. D The migration, invasion, ORO staining, and Nile red staining were performed in Huh7 cells as described in B . E , F Immunoblot detection of pmTOR level in SHIP2 E silencing in Huh7 cells or F overexpression in SNU-449 cells. G Immunoblotting of the indicated protein lysates from Huh7 cells expressing Ctrl or LINC01468 treated with or without the PIP3 inhibitor PIT-1. H Migration, invasion, ORO staining, and Nile Red staining were performed in SNU-449 cells as described in G . I Expression of LINC01468/SHIP2/mTOR cascade and Ki67 in HCC xenograft tissues. The expression of SHIP2, pmTOR, p-4E-BP1, and Ki67 was examined by IHC. Scale bars, 50 μm. Sof sorafenib, EVL everolimus (the mTOR inhibitor).

    Journal: Cell Death Discovery

    Article Title: LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2

    doi: 10.1038/s41420-022-01234-8

    Figure Lengend Snippet: Enforced expression of SHIP2 rescues the LINC01468 metabolic phenotypes. A Western blotting analysis of the SHIP2/Akt/mTOR pathway protein in SNU-449 cells cotransfected with or without shLINC01468, together with shSHIP2 or empty vector. B Migration, invasion, ORO staining, and Nile Red staining were performed in SNU-449 cells as described in A . C Western blotting analysis of the SHIP2/Akt/mTOR pathway protein in Huh7 cells cotransfected with LINC01468 or the control, together with SHIP2 or empty vector. D The migration, invasion, ORO staining, and Nile red staining were performed in Huh7 cells as described in B . E , F Immunoblot detection of pmTOR level in SHIP2 E silencing in Huh7 cells or F overexpression in SNU-449 cells. G Immunoblotting of the indicated protein lysates from Huh7 cells expressing Ctrl or LINC01468 treated with or without the PIP3 inhibitor PIT-1. H Migration, invasion, ORO staining, and Nile Red staining were performed in SNU-449 cells as described in G . I Expression of LINC01468/SHIP2/mTOR cascade and Ki67 in HCC xenograft tissues. The expression of SHIP2, pmTOR, p-4E-BP1, and Ki67 was examined by IHC. Scale bars, 50 μm. Sof sorafenib, EVL everolimus (the mTOR inhibitor).

    Article Snippet: Normal human hepatocyte THLE2 and the HCC cell lines (Huh7, SNU-449, SNU-182, and HCC-LM3) were obtained from the American Type Culture Collection (ATCC, USA) (Supplementary Table ).

    Techniques: Expressing, Western Blot, Plasmid Preparation, Migration, Staining, Over Expression, Immunohistochemistry

    LINC01468 is especially upregulated in liver tissues during NAFLD-HCC. A Heatmap summarizing RNA-Seq data for human HCC with or without NAFLD with 5944 upregulated genes (pink) and 104 downregulated genes (green). B Overlapping of the 17 genes significantly altered in both human ( n = 3) and mice ( n = 3) NAFLD-HCC ( P

    Journal: Cell Death Discovery

    Article Title: LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2

    doi: 10.1038/s41420-022-01234-8

    Figure Lengend Snippet: LINC01468 is especially upregulated in liver tissues during NAFLD-HCC. A Heatmap summarizing RNA-Seq data for human HCC with or without NAFLD with 5944 upregulated genes (pink) and 104 downregulated genes (green). B Overlapping of the 17 genes significantly altered in both human ( n = 3) and mice ( n = 3) NAFLD-HCC ( P

    Article Snippet: Normal human hepatocyte THLE2 and the HCC cell lines (Huh7, SNU-449, SNU-182, and HCC-LM3) were obtained from the American Type Culture Collection (ATCC, USA) (Supplementary Table ).

    Techniques: RNA Sequencing Assay, Mouse Assay

    LINC01468 silencing suppresses the chemoresistance of HCC cells and inhibits HCC tumorigenesis by lipid metabolism. A CCK8 assays in SNU-449 and HCC-LM3 cells transfected with or without shLINC01468. B Representative images (left panel) and number (right panel) of migratory or invasive cells transfected with the scrambled control or shLINC01468. C Representative images (left panel), weight (middle panel), and growth (right panel) of xenografts derived from HCC cells stably transfected with the scrambled control or shLINC01468. D The viability of SNU-449 cells transfected with shLINC01468 or scrambled control in the presence of different concentrations of lenvatinib (LVB) treatment was examined by the CCK8 assay. E A representative image of colony formation of SNU-449 cells transfected with shLINC01468 or scrambled control after treatment with 5 μM LVB. F , G Representative tumor images ( F ) and tumor growth curves ( G ) of xenografts derived from SNU-449 cells stably transfected with shLINC01468 or scrambled control in the presence or absence of intraperitoneal LVB injections. The right flanks of all the mice were subcutaneously injected with 5 × 10 6 cells. The tumors were collected after 4 weeks. H Viability of Huh7 cells transfected with LINC01468 or Ctrl in the presence of different concentrations of sorafenib was examined by the CCK8 assay. I A representative image of colony formation of Huh7 cells transfected with LINC01468 or Ctrl after treatment with 20 μg/mL of sorafenib. J , K Representative tumor images ( J ) and tumor growth curves ( K ) of xenografts derived from Huh7 cells stably transfected with LINC01468 or control in the presence or absence of intraperitoneal injections of 20 μg/mL sorafenib. The right flanks of the mice were subcutaneously injected with 5 × 10 6 cells. The tumors were collected after 4 weeks. The data represent the means ± S. D (* P

    Journal: Cell Death Discovery

    Article Title: LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2

    doi: 10.1038/s41420-022-01234-8

    Figure Lengend Snippet: LINC01468 silencing suppresses the chemoresistance of HCC cells and inhibits HCC tumorigenesis by lipid metabolism. A CCK8 assays in SNU-449 and HCC-LM3 cells transfected with or without shLINC01468. B Representative images (left panel) and number (right panel) of migratory or invasive cells transfected with the scrambled control or shLINC01468. C Representative images (left panel), weight (middle panel), and growth (right panel) of xenografts derived from HCC cells stably transfected with the scrambled control or shLINC01468. D The viability of SNU-449 cells transfected with shLINC01468 or scrambled control in the presence of different concentrations of lenvatinib (LVB) treatment was examined by the CCK8 assay. E A representative image of colony formation of SNU-449 cells transfected with shLINC01468 or scrambled control after treatment with 5 μM LVB. F , G Representative tumor images ( F ) and tumor growth curves ( G ) of xenografts derived from SNU-449 cells stably transfected with shLINC01468 or scrambled control in the presence or absence of intraperitoneal LVB injections. The right flanks of all the mice were subcutaneously injected with 5 × 10 6 cells. The tumors were collected after 4 weeks. H Viability of Huh7 cells transfected with LINC01468 or Ctrl in the presence of different concentrations of sorafenib was examined by the CCK8 assay. I A representative image of colony formation of Huh7 cells transfected with LINC01468 or Ctrl after treatment with 20 μg/mL of sorafenib. J , K Representative tumor images ( J ) and tumor growth curves ( K ) of xenografts derived from Huh7 cells stably transfected with LINC01468 or control in the presence or absence of intraperitoneal injections of 20 μg/mL sorafenib. The right flanks of the mice were subcutaneously injected with 5 × 10 6 cells. The tumors were collected after 4 weeks. The data represent the means ± S. D (* P

    Article Snippet: Normal human hepatocyte THLE2 and the HCC cell lines (Huh7, SNU-449, SNU-182, and HCC-LM3) were obtained from the American Type Culture Collection (ATCC, USA) (Supplementary Table ).

    Techniques: Transfection, Derivative Assay, Stable Transfection, CCK-8 Assay, Mouse Assay, Injection

    LINC01468 directly binds with SHIP2. A RNA pull-down assay flowchart was used to identify LINC01468-associated proteins. B The biotinylated LINC01468-associated proteins were stained with silver, and the bands specifically precipitated by LINC01468 were excised and submitted for mass spectrometry (top) and western blot (bottom) analysis. The arrows indicate SHIP2 proteins as the unique bands for LINC01468. C The interaction of SHIP2 and LINC01468 was analyzed by western blot. D RIP assay was performed to detect LINC01468 enrichment in the immunoprecipitated complexes using anti-SHIP2 antibodies. E FISH and IF assays were performed to determine the co-localization of LINC01468 (Cy3; red) and SHIP2 (green) in cells. Nuclei, blue (DAPI). F Diagrams of full-length LINC01468 and its deletion fragments of the SHIP2-binding domain in LINC01468. G SHIP2 pulled down by different LINC01468 constructs was tested by western blot. H The expression analysis of SHIP2 from 26 pairs of HCC tissues and corresponding para-cancerous tissues from human NAFLD-HCC by qRT-PCR. I Western blot analysis of SHIP2 in human NAFLD-associated HCC. Representative western blot images and expression levels of tumors (T) and adjacent nontumors (NT) from eight paired NAFLD-associated HCCs. J Pearson correlation analysis of LINC01468 and SHIP2 expression in 26 HCC tissues. K , L SHIP2 protein expression in palmitic acid- ( K ) or oleic acid-treated ( L ) SNU-182 cells ( n = 3 per group). ** P

    Journal: Cell Death Discovery

    Article Title: LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2

    doi: 10.1038/s41420-022-01234-8

    Figure Lengend Snippet: LINC01468 directly binds with SHIP2. A RNA pull-down assay flowchart was used to identify LINC01468-associated proteins. B The biotinylated LINC01468-associated proteins were stained with silver, and the bands specifically precipitated by LINC01468 were excised and submitted for mass spectrometry (top) and western blot (bottom) analysis. The arrows indicate SHIP2 proteins as the unique bands for LINC01468. C The interaction of SHIP2 and LINC01468 was analyzed by western blot. D RIP assay was performed to detect LINC01468 enrichment in the immunoprecipitated complexes using anti-SHIP2 antibodies. E FISH and IF assays were performed to determine the co-localization of LINC01468 (Cy3; red) and SHIP2 (green) in cells. Nuclei, blue (DAPI). F Diagrams of full-length LINC01468 and its deletion fragments of the SHIP2-binding domain in LINC01468. G SHIP2 pulled down by different LINC01468 constructs was tested by western blot. H The expression analysis of SHIP2 from 26 pairs of HCC tissues and corresponding para-cancerous tissues from human NAFLD-HCC by qRT-PCR. I Western blot analysis of SHIP2 in human NAFLD-associated HCC. Representative western blot images and expression levels of tumors (T) and adjacent nontumors (NT) from eight paired NAFLD-associated HCCs. J Pearson correlation analysis of LINC01468 and SHIP2 expression in 26 HCC tissues. K , L SHIP2 protein expression in palmitic acid- ( K ) or oleic acid-treated ( L ) SNU-182 cells ( n = 3 per group). ** P

    Article Snippet: Normal human hepatocyte THLE2 and the HCC cell lines (Huh7, SNU-449, SNU-182, and HCC-LM3) were obtained from the American Type Culture Collection (ATCC, USA) (Supplementary Table ).

    Techniques: Pull Down Assay, Staining, Mass Spectrometry, Western Blot, Immunoprecipitation, Fluorescence In Situ Hybridization, Binding Assay, Construct, Expressing, Quantitative RT-PCR

    LINC01468 activates Akt/mTOR signaling pathway. A Differently expressed genes in SNU-449 cells transfected with shLINC01468 or control were shown by heatmap. B KEGG pathway analysis of LINC01468-regulated genes. C KEGG pathway enrichment analysis of target genes by a bubble chart. The size and color of the dots represents the number and level of genes that were enriched in the corresponding pathways, respectively. D The item was enriched using GSEA in SUN-449 cells transfected with shLINC01468 or control. E , F Immunoblot detection of Akt/mTOR signaling pathway protein level in E LINC01468-knockdown SNU-449 cells or F LINC01468-overexpressed Huh7 cells. G Immunoblotting of the indicated protein lysates from Huh7 cells expressing Ctrl or LINC01468 treated with or without rapamycin (Rapa). H The intracellular lipid droplets in SUN-449 cells transfected with shLINC01468 or control were stained with oil red O. I The cellular content of triglycerides and phospholipids in the indicated cells in H was detected. J Representative liver images (top), H E staining (middle), and ORO staining (bottom) of xenografts derived from SUN-449 cells stably transfected with the scrambled control or siLINC01468. K – M Overexpression of LINC01468 increased tumor growth and mediated sorafenib resistance of HCC tumors in nude mice. Images show representative tumor ( K ). Growth curves ( L ) and tumor weights ( M ) of mean ± SD of six mice in each group.*** P

    Journal: Cell Death Discovery

    Article Title: LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2

    doi: 10.1038/s41420-022-01234-8

    Figure Lengend Snippet: LINC01468 activates Akt/mTOR signaling pathway. A Differently expressed genes in SNU-449 cells transfected with shLINC01468 or control were shown by heatmap. B KEGG pathway analysis of LINC01468-regulated genes. C KEGG pathway enrichment analysis of target genes by a bubble chart. The size and color of the dots represents the number and level of genes that were enriched in the corresponding pathways, respectively. D The item was enriched using GSEA in SUN-449 cells transfected with shLINC01468 or control. E , F Immunoblot detection of Akt/mTOR signaling pathway protein level in E LINC01468-knockdown SNU-449 cells or F LINC01468-overexpressed Huh7 cells. G Immunoblotting of the indicated protein lysates from Huh7 cells expressing Ctrl or LINC01468 treated with or without rapamycin (Rapa). H The intracellular lipid droplets in SUN-449 cells transfected with shLINC01468 or control were stained with oil red O. I The cellular content of triglycerides and phospholipids in the indicated cells in H was detected. J Representative liver images (top), H E staining (middle), and ORO staining (bottom) of xenografts derived from SUN-449 cells stably transfected with the scrambled control or siLINC01468. K – M Overexpression of LINC01468 increased tumor growth and mediated sorafenib resistance of HCC tumors in nude mice. Images show representative tumor ( K ). Growth curves ( L ) and tumor weights ( M ) of mean ± SD of six mice in each group.*** P

    Article Snippet: Normal human hepatocyte THLE2 and the HCC cell lines (Huh7, SNU-449, SNU-182, and HCC-LM3) were obtained from the American Type Culture Collection (ATCC, USA) (Supplementary Table ).

    Techniques: Transfection, Expressing, Staining, Derivative Assay, Stable Transfection, Over Expression, Mouse Assay