scholarly journals HepG2 hepatocellular carcinoma cells are a non-permissive system for B19 virus infection

2008 ◽  
Vol 89 (12) ◽  
pp. 3034-3038 ◽  
Author(s):  
Francesca Bonvicini ◽  
Claudia Filippone ◽  
Elisabetta Manaresi ◽  
Marialuisa Zerbini ◽  
Monica Musiani ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Virus Infection ◽  
Hepg2 Cells ◽  
Parvovirus B19 ◽  
Model System ◽  
Carcinoma Cells ◽  
Genome Replication ◽  
Hepatocellular Carcinoma Cells ◽  
Viral Genome Replication ◽  
Representative Model

Parvovirus B19 has been associated with liver dysfunction and has been considered a potential aetiological agent of fulminant hepatitis and hepatitis-associated aplastic anaemia. The possible effects of B19 virus infection on the liver have been investigated using HepG2 hepatocellular carcinoma cells as a model system, but the reported results are inconsistent. To investigate this relationship further, this study followed the course of B19 virus infection of HepG2 cells in terms of viral DNA, RNA and protein production by quantitative PCR, RT-PCR and immunofluorescence assays. The data showed that B19 virus is able to bind and possibly enter HepG2 cells, but that viral genome replication or transcription is not supported and that viral proteins are not produced. As far as HepG2 cells can be considered a representative model system, any possible pathogenic role of B19 virus on the liver cannot be ascribed to infection or to a direct cytopathic effect on hepatocytes.

scholarly journals Sodium citrate inhibits proliferation and induces apoptosis of hepatocellular carcinoma cells

2020 ◽  
Vol 7 (3) ◽  
pp. 3659-3666
Author(s):  
Phuc Hong Vo ◽  
Sinh Truong Nguyen ◽  
Nghia Minh Do ◽  
Kiet Dinh Truong ◽  
Phuc Van Pham
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cancer Cells ◽  
Dna Fragmentation ◽  
Hepg2 Cells ◽  
Annexin V ◽  
Carcinoma Cells ◽  
Human Gastric Cancer ◽  
Apoptosis Pathway ◽  
Hepatocellular Carcinoma Cells ◽  
Activation Assay

Introduction: Cancer cells rely on glycolysis to generate energy and synthesize biomass for cell growth and proliferation (the Warburg effect). Recent studies have shown that citrate has an inhibitory effect on several cancer cells, such as human gastric cancer and ovarian cancer, by inhibiting glycolysis. In this study, we investigated the effects of citrate on the proliferation and apoptosis induction of hepatocellular carcinoma cells. Methods: HepG2 hepatocellular carcinoma cell line was used in this study. The cell proliferation was evaluated by Alamar blue assay. The apoptotic status of the HepG2 cells was recorded by Annexin V/7-AAD assay and caspase 3/7 activation assay. DNA fragmentation was evaluated by nucleus staining assay with Hoechst 33342. Results: The results showed that citrate is able to inhibit the proliferation of HepG2 cells and induce apoptosis in these cells. The initiation time of apoptosis is 4 hours after treatment with 10 mM citrate. Morphology characteristics of DNA fragmentation and broken membranes were also recorded in the apoptotic cells. Conclusion: In conclusion, our study demonstrates that citrate causes HepG2 cell death by the apoptosis pathway.

scholarly journals Suppression of CUGBP1 inhibits growth of hepatocellular carcinoma cells

2014 ◽  
Vol 37 (1) ◽  
pp. 10 ◽  
Author(s):  
Yong Liu ◽  
Hai Huang ◽  
Bo Yuan ◽  
Tianping Luo ◽  
Jianchao Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Rna Binding ◽  
Cyclin B1 ◽  
Carcinoma Cells ◽  
Human Hepatocellular Carcinoma ◽  
Phase Cell ◽  
Hepatic Tissue ◽  
Tissue Samples ◽  
Hepatocellular Carcinoma Cells

Purpose: The multifunctional RNA-binding protein, CUGBP1, regulates splicing, stability and translation of mRNAs. Previous studies have shown that CUGBP1 is expressed at high levels in the liver, although its role in hepatocellular carcinoma is unknown. Our aim was to determine if CUGBP1 could regulate hepatocellular carcinoma growth. Methods: Expression levels of CUGBP1 were analyzed in 70 hepatic carcinoma and 20 normal hepatic tissue samples by immunohistochemistry (IHC). Using lentivirus-mediated short hairpin RNA (shRNA), CUGBP1 expression in human hepatocellular carcinoma HepG2 cells was knocked-down. The effect of CUGBP1 on hepatic cancer cell growth was investigated. Results: CUGBP1 was expressed in 85.7% hepatocellular carcinoma specimens compared with 50% in normal liver specimens. CUGBP1 silencing remarkably decreased the proliferation of HepG2 cells, as determined by MTT assay. Flow cytometry analysis showed that knock-down of CUGBP1 led to G0/G1 phase cell cycle arrest, accompanied by sub-G1 accumulation. Moreover, depletion of CUGBP1 resulted in downregulation of cyclin B1 and upregulation of cyclin D1. Conclusion: These results suggest that CUGBP1 is essential for the growth of hepatocellular carcinoma cells. Knockdown of CUGBP1 might be a potential therapeutic approach for human hepatocellular carcinoma.

scholarly journals Houttuynia cordata Thunb Promotes Activation of HIF-1A–FOXO3 and MEF2A Pathways to Induce Apoptosis in Human HepG2 Hepatocellular Carcinoma Cells

2016 ◽  
Vol 16 (3) ◽  
pp. 360-372 ◽  
Author(s):  
Jung Min Kim ◽  
In-Hu Hwang ◽  
Ik-Soon Jang ◽  
Min Kim ◽  
In Seok Bang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Hypoxia Inducible Factor ◽  
Carcinoma Cells ◽  
Houttuynia Cordata ◽  
Hepatocellular Carcinoma Cells ◽  
Human Liver Cancer ◽  
Houttuynia Cordata Thunb ◽  
Human Liver Cancer Cells

Houttuynia cordata Thunb ( H cordata), a medicinal plant, has anticancer activity, as it inhibits cell growth and induces cell apoptosis in cancer. However, the potential anti-cancer activity and mechanism of H cordata for human liver cancer cells is not well understood. Recently, we identified hypoxia-inducible factor (HIF)-1A, Forkhead box (FOX)O3, and MEF2A as proapoptotic factors induced by H cordata, suggesting that HIF-1A, FOXO3, and MEF2A contribute to the apoptosis of HepG2 hepatocellular carcinoma cells. FOXO3 transcription factors regulate target genes involved in apoptosis. H cordata significantly increased the mRNA and protein expression of HIF-1A and FOXO3 and stimulated MEF2A expression in addition to increased apoptosis in HepG2 cells within 24 hours. Therefore, we determined the potential role of FOXO3 on apoptosis and on H cordata–induced MEF2A in HepG2 cells. HIF-1A silencing by siRNA attenuated MEF2A and H cordata–mediated FOXO3 upregulation in HepG2 cells. Furthermore, H cordata–mediated MEF2A expression enhanced caspase-3 and caspase-7, which were abolished on silencing FOXO3 with siRNA. In addition, H cordata inhibited growth of human hepatocellular carcinoma xenografts in nude mice. Taken together, our results demonstrate that H cordata enhances HIF-1A/FOXO3 signaling, leading to MEF2A upregulation in HepG2 cells, and in parallel, it disturbs the expression of Bcl-2 family proteins (Bax, Bcl-2, and Bcl-xL), which results in apoptosis. Taken together, these findings demonstrate that H cordata promotes the activation of HIF-1A–FOXO3 and MEF2A pathways to induce apoptosis in human HepG2 hepatocellular carcinoma cells and is, therefore, a promising candidate for antitumor drug development.

scholarly journals Effects of miR-489 targeting on SOX4 gene on proliferation and apoptosis of human hepatocellular carcinoma cells

2020 ◽  
Vol 20 (3) ◽  
pp. 1292-1298
Author(s):  
Bing Wang ◽  
Wang-Xun Jin ◽  
Yun-Li Zhang ◽  
Ling Huang ◽  
Hai-Bin Ni ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Liver Cancer ◽  
Hepg2 Cells ◽  
Carcinoma Cells ◽  
Human Hepatocellular Carcinoma ◽  
Hepatocellular Carcinoma Cells ◽  
Human Hepatocellular Carcinoma Cells

Background: Hepatocellular carcinoma is one of the most common malignant tumors found all over the globe. Despite advances in surgery and chemotherapy, the five-year survival rate of patients with hepatocellular carcinoma is still low. It is known that the proliferation of hepatocellular carcinoma cells is closely related to the occurrence, development and prog- nosis of hepatocellular carcinoma. The present work investigates the expression of microRNA-489 (miR-489) in human hepatocellular carcinoma cells and its effect on the biological behavior of human hepatocellular carcinoma cells. Methods: The expression of miR-489 by fluorescence quantitative PCR detection in 30 patients with hepatoblastoma of liver cancer tissues and adjacent tissues was studied. Also, the determination of hepatoblastoma in four cell lines with differ- ent metastatic potential (HR8348, HCT116, HT29 and HEPG2) and the expression of miR-489 during miR-489 simulation process was studied. MTT assay, flow cytometry and Western blot analysis were performed to know the cell proliferation to detect the changes in cell cycle, apoptosis of cells, and SOX4 gene expression respectively. Results: RT-PCR results showed that the cells compared with pre-cancerous tissue, the expression level of miR-489 in hepatocellular carcinoma tissues than in adjacent tissue significantly decreased (P<0.05), and with liver cancer cell metastasis increased (P<0.05); analogue transfection constructed miR-489 overexpressing HEPG2 cell line by microRNA. MTT results showed that miR-489 can inhibit the proliferation of HEPG2 cells, the differences were statistically significant (P<0.05); flow cytometry results showed that miR-489 mimics was transfected into HEPG2 cells at 48 hours had no significant effect on cell cycle distribution (P > 0.05); but miR-489 expression could induce apoptosis, compared with the control group, the apoptosis of miR-489 mimics was significantly increased and the difference was statistically significant (P < 0.05). Conclusion: In conclusion, miR-489 can significantly inhibit the occurrence and development of hepatocellular carcinoma cells. The mechanism may be down regulated by the expression of SOX4 and inhibit cell proliferation. Further this study showed that the tumor cells SOX4 gene as a regulatory factor target the genes of miR-489 in hepatocellular carcinoma. Keywords: Hepatocellular carcinoma; mircroRNA-489; SOX4; apoptosis.

scholarly journals Autophagy and autophagy dysfunction contribute to apoptosis in HepG2 cells exposed to nanosilica

2016 ◽  
Vol 5 (3) ◽  
pp. 871-882 ◽  
Author(s):  
Yongbo Yu ◽  
Junchao Duan ◽  
Yang Yu ◽  
Yang Li ◽  
Yang Zou ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Hepg2 Cells ◽  
Carcinoma Cells ◽  
Human Hepatocellular Carcinoma ◽  
Hepatocellular Carcinoma Cells ◽  
Icr Mice ◽  
Distinct Cell ◽  
Human Hepatocellular Carcinoma Cells

The present study investigated both autophagy and apoptosis in ICR mice and Human hepatocellular carcinoma cells (HepG2), and then explored the interactive mechanism between these two distinct cell death modalities in HepG2 cells.

Effect of the BBC3 Gene on the Proliferation and Apoptosis of Hepatocellular Carcinoma Cells Through p53-Regulated Signaling

2021 ◽  
Vol 11 (1) ◽  
pp. 135-141
Author(s):  
Sheng Zheng ◽  
Hua Yang ◽  
Yefei Chang ◽  
Dan Zhao ◽  
Juan Yang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Hepg2 Cell ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Carcinoma Cells ◽  
Caspase 9 ◽  
Hepatocellular Carcinoma Cells ◽  
P53 Signaling ◽  
Normal Human Liver

We examined the effect of the BBC3 gene on hyperplasia and apoptosis in HepG2 cells and its underlying mechanism. Quantitative RT-PCR was used to determine the level of BBC3 expression in HL-7702 normal human liver cells and four different hepatocellular carcinoma cell lines (HepG2, HuH-7, HCCLM3 and MHCC97H). Transfection was performed with Lipofectamine 2000 reagent and the transfectants were divided into three groups: pcDNA-BBC3 group (transfected BBC3 over-expressing plasmid), pcDNA-NC group (transfected empty plasmid), and a Ctrl group (not transfected). Quantitative RT-PCR and western blot analysis were used to measure BBC3 expression. The CCK-8 assay was used to determine the effect of BBC3 on HepG2 cell proliferation. Flow cytometry was used for testing the effect of overexpressing BBC3 on apoptosis in HepG2 cells. The levels of cleaved-Caspase-3 (C-Caspase-3), cleaved-Caspase-9 (C-Caspase-9), and proteins associated with the p53 signaling pathway were assessed by western blot analysis. The level of BBC3 mRNA in HL-7702 normal human liver cells was significantly higher compared with that in human hepatocellular carcinoma cells including HepG2, HuH-7, HCCLM3 and MHCC97H (P < 0.05). The lowest level of BBC3 mRNA was observed in HepG2 cells. The level of BBC3 mRNA and protein in HepG2 cells were significantly higher compared with that of the pcDNA-NC group following transfection with a BBC3 overexpressing plasmid. HepG2 cell proliferation in the pcDNA-NC group was higher compared with that of the pcDNA-BBC3-transfected group (P < 0.05). The apoptotic rate and levels of cleaved-Caspase-3, cleaved-Caspase-9, p53, phospho-p53, and p21 protein in cells were higher compared with that of the pcDNA-NC group. No change was observed in the pcDNA-NC and Ctrl groups. The BBC3 gene was down-regulated in hepatocellular carcinoma cells. HepG2 cell proliferation can be inhibited and HepG2 cell apoptosis can be induced by the overexpression of BBC3 through activation of the p53 signaling pathway.

scholarly journals Anti-Tumor Activity of Cembranoid-Type Diterpenes Isolated from Nicotiana tabacum L.

Biomolecules ◽  
2019 ◽  
Vol 9 (2) ◽  
pp. 45 ◽  
Author(s):  
Xiao-Long Yuan ◽  
Xin-Xin Mao ◽  
Yong-Mei Du ◽  
Pei-Zhen Yan ◽  
Xiao-Dong Hou ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Nicotiana Tabacum ◽  
Hepg2 Cells ◽  
Hepatoma Cell ◽  
Antitumor Agent ◽  
Carcinoma Cells ◽  
Altered Expression ◽  
Hepatocellular Carcinoma Cells ◽  
Nicotiana Tabacum L ◽  
Anti Tumor Activity

Recently, the incidence of hepatocellular carcinoma has increased worldwide. Cembranoid-type diterpenes (CBDs) from tobacco exhibit good antimicrobial, antitumor, and neuroprotective activities. Therefore, in this study, we isolated CBDs from Nicotiana tabacum L. and evaluated their antitumor activity against hepatoma cell lines. Particularly, the anti-tumor activity of α-2,7,11-cyprotermine-4,6-diol (α-CBD) was investigated against HepG2, SMMC-7721, and HL-7702 cells. The MTT assay revealed that α-CBD reduced the formation of cell clones and inhibited the proliferation of hepatocellular carcinoma cells. Morphological observations showed that α-CBD altered cell morphology and membrane permeability before inducing apoptosis. To further explore the antitumor mechanism of α-CBD, flow cytometry and transcriptome analysis were performed using HepG2 cells. The results showed that the number of HepG2 cells increased from 10.4% to 29.8%, indicating that α-CBD inhibits the proliferation of hepatocellular carcinoma cells in the S phase. The gene expression analysis of HepG2 cells treated with α-CBD showed 3068 genes with altered expression, among which 1289 were upregulated and 1779 were downregulated. Apoptosis induced by these differentially expressed genes might be mediated by the p53-PUMA, PI3K-Akt, and IL-1-NF-κB-IAP pathways. Comprehensively, our study shows that α-CBD isolated from N. tabacum L. can be potentially used as a natural antitumor agent.

In Vitro Investigation of Therapeutic Potential of Bare Magnetite (Fe3O4) Nanoparticles (≤100 ppm) on Hepatocellular Carcinoma Cells

2020 ◽  
Vol 20 (3) ◽  
pp. 1391-1400 ◽  
Author(s):  
Kurtulus Gokduman ◽  
Asiye Gok
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Cells ◽  
Magnetite Nanoparticles ◽  
Hepg2 Cells ◽  
Biomedical Applications ◽  
Therapeutic Potential ◽  
Carcinoma Cells ◽  
Mitochondrial Activity ◽  
Ros Production ◽  
Hepatocellular Carcinoma Cells

Significant ROS production capability of bare iron oxide nanoparticles in safe doses for healthy cells offers an interesting therapeutic window for cancer. In this context, the aim of the current study is to investigate therapeutic potential of the synthesized magnetite (Fe3O4) nanoparticles (~80 nm) as attractive vehicles for biomedical applications on hepatocellular carcinoma cells (HepG2). To investigate their time (0–72 h) and dose (0–100 μg/ml) dependent effect on physiological state (proliferation/ cytotoxicity) and mitochondrial activity of the tumor cells, xCELLigence system and MTT assay were used, respectively. Both 50 and 100 μg/ml of nanoparticle treatment induced significant (p < 0.01) increases in ROS production in HepG2 cells; however, ~4-day real-time cell analysis illustrated that all concentrations of the nanoparticles caused significant (p < 0.01) increases in proliferation of the tumor cells from 4 h after the treatment to the end of the analysis. While 50 and 100 μg/ml of nanoparticles caused significant deteriorations in the mitochondrial activity of the tumor cells in the case of 24 h-(p < 0.05 and p < 0.01, respectively) and 72 h-treatment (p < 0.01); 24 h-treatment of 100 μg/ml of nanoparticles and 72 h-treatment of 50 and 100 μg/ml of nanoparticles caused significant increases in the mitochondrial activity of the tumor cells (p < 0.01) under static magnetic field (1.35 T). Although the synthesized magnetite nanoparticles have not therapeutic potential alone on HepG2 cells in doses safe for healthy cells, the results of the current study are illuminating for future magnetite nanoparticle-based biomedical applications and combination cancer therapy containing magnetite nanoparticles.

scholarly journals Preparation and Nanoencapsulation of Lectin from Lepidium sativum on Chitosan-Tripolyphosphate Nanoparticle and Their Cytotoxicity against Hepatocellular Carcinoma Cells (HepG2)

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Unzila Yasin ◽  
Muhammad Bilal ◽  
Hamid Bashir ◽  
Muhammad Imran Amirzada ◽  
Aleena Sumrin ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Carcinoma Cells ◽  
Lepidium Sativum ◽  
Cell Agglutination ◽  
Proliferation Markers ◽  
Hepatocellular Carcinoma Cells ◽  
Biological Recognition ◽  
Ic50 Values ◽  
Lectin Protein

Lectins are the oligomeric sugar-specific glycoprotein of nonimmune origin, are involved in the multiple biological recognition process, and have the capacity to perform a wide variety of physiological functions including antifungal, antiviral, antitumor, and cell agglutination. The main objective of the current study was to prepare lectin protein-loaded chitosan-TPP nanoparticles via ionic gelation methods with different CS/TPP ratios and to investigate anticancer potential against HepG2 cells. The best ratio showed the mean particle size ( 298.10 ± 1.9  nm, 21.05 ± 0.95  mv) with optimal encapsulation efficiencies of 52.435 ± 0.09 % . The cytotoxicity was evaluated against HepG2 cells, and IC50 values obtained were 265 μg/ml for lectin protein and 105 μg/ml for lectin-loaded chitosan-TPP nanoparticles, respectively. The mRNA expression of proliferation markers like GPC3 was significantly decreased in hepatocellular carcinoma cells (HepG2) during lectin protein-loaded chitosan-TPP nanoparticle treatment. Apoptotic genes that indicating a marked increase in expression are Caspase 3, p53, and Bax, while Bcl2 and AFP showed a downregulation of expression after treatment of HepG2 cells with lectin-loaded chitosan-TPP nanoparticles. The preliminary findings of our study highlighted that lectin protein-loaded chitosan-TPP nanoparticles could be a promising anticancer agent.

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