• Title/Summary/Keyword: Hep G2 cell

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Functional Gene Analysis to Identify Potential Markers Induced by Benzene in Two Different Cell Lines, HepG2 and HL-60

  • Kim, Youn-Jung;Song, Mi-Kyung;Sarma, Sailendra Nath;Choi, Han-Saem;Ryu, Jae-Chun
    • Molecular & Cellular Toxicology
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    • v.4 no.3
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    • pp.183-191
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    • 2008
  • Volatile organic compounds (VOCs) are common constituents of cleaning and degreasing agents, paints, pesticides, personal care products, gasoline and solvents. And VOCs are evaporated at room temperature and most of them exhibit acute and chronic toxicity to human. Benzene is the most widely used prototypical VOC and the toxic mechanisms of them are still unclear. The multi-step process of toxic mechanism can be more fully understood by characterizing gene expression changes induced in cells by toxicants. In this study, DNA microarray was used to monitor the expression levels of genes in HepG2 cells and HL-60 cells exposed to the benzene on IC20 and IC50 dose respectively. In the clustering analysis of gene expression profiles, although clusters of HepG2 and HL-60 cells by benzene were divided differently, expression pattern of many genes observed similarly. We identified 916 up-regulated genes and 1,144 down-regulated genes in HepG2 cells and also 1,002 up-regulated genes and 919 down-regulated genes in HL-60 cells. The gene ontology analysis on genes expressed by benzene in HepG2 and HL-60 cells, respectively, was performed. Thus, we found some principal pathways, such as, focal adhesion, gap junction and signaling pathway in HepG2 cells and toll-like receptor signaling pathway, MAPK signaling pathway, p53 signaling pathway and neuroactive ligand-receptor interaction in HL-60 cells. And we also found 16 up-regulated and 14 down-regulated commonly expressed total 30 genes that belong in the same biological process like inflammatory response, cell cycle arrest, cell migration, transmission of nerve impulse and cell motility in two cell lines. In conclusion, we suggest that this study is meaningful because these genes regarded as strong potential biomarkers of benzene independent of cell type.

Identification of matrix metalloproteinases secreted by human hepatocarcinoma HepG2 cells

  • Lee, Young Jae;Kim, Keun Cheon;Lim, Jeong Mook;Lee, Seung Tae
    • Journal of Animal Reproduction and Biotechnology
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    • v.37 no.1
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    • pp.62-66
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    • 2022
  • To date, the development of anticancer drugs has been conducted using two-dimensional (2D) cell culture systems. However, since cancer cells in the body are generated and developed in three-dimensional (3D) microenvironments, the use of 2D anticancer drug screening can make it difficult to accurately evaluate the anticancer effects of drug candidates. Therefore, as a step towards developing a cancer cell-friendly 3D microenvironment based on a combination of vinylsulfone-functionalized polyethylene glycol (PEG-VS) with dicysteine-containing crosslinker peptides with an intervening matrix metalloproteinase (MMP)-specific cleavage site, the types of MMPs secreted from human hepatocarcinoma HepG2 cells, a representative cancer cell, were analyzed transcriptionally and translationally. MMP3 was confirmed to be the most highly expressed protease secreted by HepG2 cells. This knowledge will be important in the design of a crosslinker necessary for the construction of PEG-based hydrogels customized for the 3D culture of HepG2 cells.

Growth Inhibitory and Quinone Reductase Activity Stimulating Effects of Internal Organs of Todarodes pacificus Fractions on Human Cancer Cell Lines In vitro (오징어내장 분획물의 in vitro에서의 암세포 성장억제 및 quinone reductase유도 활성 증가 효과)

  • Shin, Mi-Ok;Bae, Song-Ja
    • Journal of Life Science
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    • v.19 no.9
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    • pp.1251-1257
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    • 2009
  • We investigated the growth inhibitory effect of internal organs of Todarodes pacificus (TP) on proliferation in human cancer cell lines in vitro. The internal organs of TP were extracted with methanol (TPM), which was then further fractionated into four subfractions by using a solvent partition method, resulting in hexane (TPMH), methanol (TPMM), butanol (TPMB), and aqueous (TPMA) soluble fractions. We determined the cytotoxic effect of these four fractions in three kinds of cancer cell lines - HepG2, MCF-7 and HT-29 - by MTT assay. Among the four subfractions of TPM, TPMH showed the strongest cytotoxic effects at a concentration of $300{\mu}g$/ml, displaying 91.56% on the HepG2 cell line and 85.93% on the MCF-7 cell line. Morphological changes such as membrane shirinking and blebbing of cells were also observed during TPMH treatment of HepG2 cells. In addition, we also observed quinone reductase (QR) induced effect in the methanol (TPMM) layer of HepG2 cells. TPMM showed the highest induction activity of quinone reductase on HepG2 cells among the other partition layers. The QR induced effect of TPMM was determined to be 2.7 at a level of $360{\mu}g$/ml with a control value of 1.0. Although further studies are needed, the present work suggests that internal organs of Todarodes pacificus (TP) may be a chemopreventive agent for the treatment of human cells.

Cytotoxicity Assessments of Portulaca oleracea and Petroselinum sativum Seed Extracts on Human Hepatocellular Carcinoma Cells (HepG2)

  • Farshori, Nida Nayyar;Al-Sheddi, Ebtesam Saad;Al-Oqail, Mai Mohammad;Musarrat, Javed;Al-Khedhairy, Abdulaziz Ali;Siddiqui, Maqsood Ahmed
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.16
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    • pp.6633-6638
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    • 2014
  • The Pharmacological potential, such as antioxidant, anti-inflammatory, and antibacterial activities of Portulaca oleracea (PO) and Petroselinum sativum (PS) extracts are well known. However, the preventive properties against hepatocellular carcinoma cells have not been explored so far. Therefore, the present investigation was designed to study the anticancer activity of seed extracts of PO and PS on the human hepatocellular carcinoma cells (HepG2). The HepG2 cells were exposed with $5-500{\mu}g/ml$ of PO and PS for 24 h. After the exposure, cell viability by 3-(4,5-dimethylthiazol-2yl)-2,5-biphenyl tetrazolium bromide (MTT) assay, neutral red uptake (NRU) assay, and cellular morphology by phase contrast inverted microscope were studied. The results showed that PO and PS extracts significantly reduced the cell viability of HepG2 in a concentration dependent manner. The cell viability was recorded to be 67%, 31%, 21%, and 17% at 50, 100, 250, and $500{\mu}g/ml$ of PO, respectively by MTT assay and 91%, 62%, 27%, and 18% at 50, 100, 250, and $500{\mu}g/ml$ of PO, respectively by NRU assay. PS exposed HepG2 cells with $100{\mu}g/ml$ and higher concentrations were also found to be cytotoxic. The decrease in the cell viability at 100, 250, and $500{\mu}g/ml$ of PS was recorded as 70%, 33%, and 15% by MTT assay and 63%, 29%, and 17%, respectively by NRU assay. Results also showed that PO and PS exposed cells reduced the normal morphology and adhesion capacity of HepG2 cells. HepG2 cells exposed with $50{\mu}g/ml$ and higher concentrations of PO and PS lost their typical morphology, become smaller in size, and appeared in rounded bodies. Our results demonstrated preliminary screening of anticancer activity of Portulaca oleracea and Petroselinum sativum extracts against HepG2 cells, which can be further used for the development of a potential therapeutic anticancer agent.

Cytotoxicity of Ligularia fischeri Extracts (곰취 추출물의 세포독성 효과)

  • 함승시;이상영;오덕환;정성원;김상헌;정차권;강일준
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.27 no.5
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    • pp.987-992
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    • 1998
  • This study was investigated to observe the cytotoxicity effect of Ligularia fischeri extracts against cancer cell lines including human lung carcinoma(A549), human cervix epitheloid carcinoma(HeLa) and human hepatocellular carcinoma(HepG2) using SRB(sulforhodamine B) method. The ethanol and methanol extracts of 1$\mu\textrm{g}$/${mu}ell$ showed approximately 79.2% and 86.4% cytotoxicity effects on HepG2 cell line and the ethyl acetate fracton fractionated from ethanol extracts showed the strongest cytotoxicity effect with 94% inhibition. The inhibitory effect of ethanol extract on HeLa cell line was somewhat low with 50~56% inhibition, but ethyl acetate fraction showed higher cytotoxicity effect with 91% and 91.9% inhibition on the HeLa and A549 cell line. On the contrary, the ethanol and methanol extracts showed the lower inhibition effects on the normal liver cell, WRL68, compared to human cancer cell lines.

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Effects of Cholic Acid/CDCA and FGF-19 on the Protein Levels of the Endogenous Small Heterodimer Partner (SHP) in the Mouse Liver and HepG2 Cells (생쥐의 간과 HepG2 세포에 있어서 내인성 small heterodimer partner (SHP)의 단백질 수준에 미치는 cholic acid/CDCA 및 FGF-19의 효과)

  • Min, Gye-Sik
    • Journal of Life Science
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    • v.19 no.12
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    • pp.1731-1736
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    • 2009
  • Recent studies determined that a chronic western-style diet increased the endogenous small heterodimer partner (SHP) protein levels in mice. In experiments with cell cultures, chenodeoxy cholic acid (CDCA) treatment increased endogenous SHP protein levels and reduced the degradation rate of exogenously expressed flag-SHP levels in the human hepatoma cell line, HepG2 cells. In addition, bile acid-induced intestinal fibroblast growth factor-19 (FGF-19) increased the half-life of the exogenously expressed SHP when HepG2 cells were transfected with ad-flag-SHP. However, both the expression level and the degradation rate of the endogenous SHP in response to cholic acid and FGF-19 have not been well understood, either in mice or in cultured HepG2 cells. This study examined the effects of cholic acid treatment on the endogenous SHP protein levels in mice and the effects of FGF-19 on the degradation rate of the endogenous SHP protein in HepG2 cells. Mice fed 0.5% cholic acid in normal chow showed an increase in endogenous SHP protein levels during both 12 hr and 24 hr treatment periods as compared to control mice fed only normal chow. In cultured HepG2 cells, treatment with CDCA did not noticeably change the rate of degradation in the endogenous SHP protein from cells not treated with CDCA. Although consistent with the previous studies on the exogenous ad-flag-SHP protein, treatment with FGF-19 significantly decreased the degradation rate of the endogenous SHP protein when HepG2 cells were treated with cyclohexamide. These results suggest that both bile acids and FGF-19 increase the endogenous SHP protein levels in mouse liver and HepG2 cells.

In vitro Anticancer Effect of Salt on HepG2 Human Hepatocellular Carcinoma Cells (소금의 HepG2 인체 간암세포에서의 in vitro 항암 효과)

  • Kim, Hee-Young;Ju, Jaehyun;Lee, Kyung Hee;Park, Kun-Young
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.45 no.1
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    • pp.137-142
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    • 2016
  • We investigated the anti-proliferative effects of solar salt and purified salt (PS) on HepG2 human hepatocellular cancer cells as well as their effects on mRNA and protein expression of apoptosis- and cell cycle-related genes, including Bcl-2, Bax, p53, and p21. Each salt sample suppressed cancer cell proliferation when treated at a concentration of 0.5% or 1%. Especially solar salt from T salt field (SS-T) and solar salt from Y salt field (SS-Y) significantly suppressed proliferation of cancer cells in comparison with PS. Treatment of HepG2 cells with salt samples at a concentration of 1% suppressed expression of Bcl-2 and promoted expression of Bax, p53, and p21 at the mRNA and protein levels in comparison with the control group. Inductively coupled plasma optical emission spectrometry (ICP-OES) showed that SS-T and SS-Y had higher concentrations of Ca, Mg, S, and K than PS, and SS-T contained higher concentrations of these minerals than SS-Y. It seems that Na and mineral contents in solar salt may contribute to regulation of the genes. Taken together, salt, especially mineral rich solar salt, inhibits cancer cell growth by regulating apoptosis and cell cycle-related genes.

Dihydroartemisinin inhibits HepG2.2.15 proliferation by inducing cellular senescence and autophagy

  • Zou, Jiang;Ma, Qiang;Sun, Ru;Cai, Jiajing;Liao, Hebin;Xu, Lei;Xia, Jingruo;Huang, Guangcheng;Yao, Lihua;Cai, Yan;Zhong, Xiaowu;Guo, Xiaolan
    • BMB Reports
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    • v.52 no.8
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    • pp.520-525
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    • 2019
  • Dihydroartemisinin (DHA) has been reported to possess anti-cancer activity against many cancers. However, the pharmacologic effect of DHA on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Thus, the objective of the present study was to determine whether DHA could inhibit the proliferation of HepG2.2.15 cells and uncover the underlying mechanisms involved in the effect of DHA on HepG2.2.15 cells. We found that DHA effectively inhibited HepG2.2.15 HCC cell proliferation both in vivo and in vitro. DHA also reduced the migration and tumorigenicity capacity of HepG2.2.15 cells. Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, ${\gamma}-H_2AX$, P53, and P21 involved in DNA damage response. DHA also induced autophagy (green LC3 puncta gathered together and LC3II/LC3I ratio increased through AKT-mTOR pathway suppression). Results also revealed that DHA-induced autophagy was not linked to senescence or cell death. TPP1 (telomere shelterin) overexpression could not rescue DHA-induced anticancer activity (cell proliferation). Moreover, DHA down-regulated TPP1 expression. Gene knockdown of TPP1 caused similar phenotypes and mechanisms as DHA induced phenotypes and mechanisms in HepG2.2.15 cells. These results demonstrate that DHA might inhibit HepG2.2.15 cells proliferation through inducing cellular senescence and autophagy.

Induction of Apoptosis by Bile Acids in HepG2 Human Hepatocellular Carcinoma Cells

  • Baek, Jin-Hyen;Kim, Jung-Ae;Kang, Chang-Mo;Lee, Yong-Soo;Kim, Kyu-Won
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.1
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    • pp.107-115
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    • 1997
  • We studied the effects of bile acids on the induction ofapoptosis in HepG2 human hepatocellular carcinoma cells. Treatment with either ursodeoxycholic acid (UDCA) or lithocholic acid (LCA) resulted in a dose- and time-dependent decrease in cell viability assessed by MTT assay. Both UDCA and LCA also induced genomic DNA fragmentation, a hallmark of apoptosis, indicating that the mechanism by which these bile acids induce cell death was through apoptosis. Cycloheximide, a protein synthesis inhibitor, blocked the apoptosis induced by these bile acids, implying that new protein synthesis may be required for the apoptosis. Intracellular $Ca^{2+}$ release blockers (dantrolene and 3,4,5-trimethoxybenzoic acid-8-(diethylamino)octyl ester) inhibited decreased cell viability and DNA fragmentation induced by these bile acids. Treatment of HepG2 cells with calcium ionophore A23l87 induced DNA fragmentation. These results suggest that UDCA and LCA induce apoptosis in the HepG2 cells and that the activation of intracellular $Ca^{2+}$ signals may play an important role in the apoptosis induced by these bile acids.

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EGF Reverses Multi-drug Resistance via the p-ERK Pathway in HepG2/ADM and SMMC7721/ADM Hepatocellular Carcinoma Models

  • Yan, Feng;Bai, Li-Ping;Gao, Hua;Zhu, Chang-Ming;Lin, Li;Kang, Xiang-Peng
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.6
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    • pp.2619-2623
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    • 2014
  • Aim: To investigate signaling pathways for reversal of EGF-mediated multi-drug resistance (MDR) in hepatocellular carcinoma (HCC) models. Materials and Methods: HCC MDR cell strain HepG2/adriamycin (ADM) and SMMC7721/ADM models were established using a method of exposure to medium with ADM between low and high concentration with gradually increasing concentration. Drug sensitivity and reversal of multi-drug resistance by EGF were determined and the cell cycle distribution and apoptosis were analyzed by flow cytometry. Phosphorylation of ERK1, ERK2, ERK5 and expression of Bim were detected by Western blotting. Results: The results showed that HepG2/ADM and SMMC7721/ADM cells were resistant not only to ADM, but also to multiple anticancer drugs. When used alone, EGF had no anti-tumor activity in HepG2/ADM and SMMC7721/ADM cells in vitro, while it increased the cytotoxicity of ADM. EGF induced cell apoptosis and G0/G1 phase cell cycle arrest in HepG2/ADM And SMMC7721/ADM cells, while enhancing activity of p-ERKs and up-regulated expression of BimEL. Conclusions: EGF might enhance the chemosensitivity of HepG2/ADM and SMMC7721/ADM cells via up-regulating p-ERKs and BimEL protein.