scholarly journals PJ34, an inhibitor of PARP-1, suppresses cell growth and enhances the suppressive effects of cisplatin in liver cancer cells

1994 ◽  
Author(s):  
Huang
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Liver Cancer Cells ◽  
Parp 1

19-Nor-2α-(3-hydroxypropyl)-1α,25-dihydroxyvitamin D3 (MART-10) is a potent cell growth regulator with enhanced chemotherapeutic potency in liver cancer cells

Steroids ◽  
2011 ◽  
Vol 76 (13) ◽  
pp. 1513-1519 ◽  
Author(s):  
Kun-Chun Chiang ◽  
Chun-Nan Yeh ◽  
Huang-Yang Chen ◽  
Jim-ming Lee ◽  
Horng-Heng Juang ◽  
...  
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Growth Regulator ◽  
Dihydroxyvitamin D3 ◽  
Liver Cancer Cells

Activation of PPARΓ inhibits cell growth and induces apoptosis in human liver cancer cells

2000 ◽  
Vol 118 (4) ◽  
pp. A921
Author(s):  
Mitsuo Toyoda ◽  
Hitoshi Takagi ◽  
Norio Horiguchi ◽  
Hisashi Takayama ◽  
Ken Sato ◽  
...  
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Human Liver ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

scholarly journals Methionine Supplementation Affects Metabolism and Reduces Tumor Aggressiveness in Liver Cancer Cells

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2491
Author(s):  
Farida Tripodi ◽  
Beatrice Badone ◽  
Marta Vescovi ◽  
Riccardo Milanesi ◽  
Simona Nonnis ◽  
...  
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Tca Cycle ◽  
Central Carbon Metabolism ◽  
Main Role ◽  
Atp Production ◽  
Liver Cancer Cells ◽  
Methionine Supplementation

Liver cancer is one of the most common cancer worldwide with a high mortality. Methionine is an essential amino acid required for normal development and cell growth, is mainly metabolized in the liver, and its role as an anti-cancer supplement is still controversial. Here, we evaluate the effects of methionine supplementation in liver cancer cells. An integrative proteomic and metabolomic analysis indicates a rewiring of the central carbon metabolism, with an upregulation of the tricarboxylic acid (TCA) cycle and mitochondrial adenosine triphosphate (ATP) production in the presence of high methionine and AMP-activated protein kinase (AMPK) inhibition. Methionine supplementation also reduces growth rate in liver cancer cells and induces the activation of both the AMPK and mTOR pathways. Interestingly, in high methionine concentration, inhibition of AMPK strongly impairs cell growth, cell migration, and colony formation, indicating the main role of AMPK in the control of liver cancer phenotypes. Therefore, regulation of methionine in the diet combined with AMPK inhibition could reduce liver cancer progression.

scholarly journals Sinusoidal swinging dynamics of the telomere repair and cell growth activation functions of telomerase in rat liver cancer cells

FEBS Letters ◽  
2006 ◽  
Vol 581 (1) ◽  
pp. 125-130 ◽  
Author(s):  
Claire Wolfrom ◽  
Olivier C. Martin ◽  
Michel Laurent ◽  
Jean Deschatrette
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Rat Liver ◽  
Activation Functions ◽  
Liver Cancer Cells ◽  
Growth Activation

scholarly journals mir-182-5p Regulates Cell Growth of Liver Cancer via Targeting RCAN1

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jianxing Zheng ◽  
Dongyang Wu ◽  
Libing Wang ◽  
Fengzhi Qu ◽  
Daming Cheng ◽  
...  
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Reliable Data ◽  
Potential Mechanism ◽  
Cycle Progression ◽  
Liver Cancer Cells ◽  
Upstream Regulator ◽  
Endogenous Protein

Regulator of calcineurin 1 (RCAN1) is an endogenous protein that is involved in the regulation of the occurrence and progression of a variety of cancers, but currently, people know little about its potential mechanism. This study investigated the function and mechanism of RCAN1 and miR-182-5p in liver cancer cells. In this study, reliable data demonstrated that RCAN1 suppressed cell proliferation, migration, invasion, and cell cycle progression of liver cancer. Additionally, the expression of RCAN1 was noted to be regulated by its upstream regulator miR-182-5p, and miR-182-5p was prominently highly expressed in liver cancer cells. Based on this, it was further proved through cell experiments that miR-182-5p facilitated cell growth of liver cancer through RCAN1 downregulation, showing that RCAN1 may be a fresh biomarker and target for diagnosis and treatment of liver cancer.

scholarly journals BRUNOL5 as a Novel Oncogene Is Epigenetically Regulated by Stilbenoids in Primary Liver Cancer Cells

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 287-287
Author(s):  
Tony Yang ◽  
Cayla Boycott ◽  
Katarzyna Lubecka ◽  
Barbara Stefanska
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Rna Sequencing ◽  
Hepg2 Cells ◽  
Primary Liver Cancer ◽  
Liver Cancer Cells ◽  
Anti Cancer

Abstract Objectives We previously discovered that a novel gene, BRUNOL5, is hypomethylated at the promoter region and upregulated in patients with primary liver cancer. Since DNA hypomethylation was shown to underlie up-regulation of genes with oncogenic functions, BRUNOL5 could potentially act as an oncogene. Interestingly, certain dietary compounds such as polyphenols with a stilbenoid ring have been demonstrated by us and others to suppress hypomethylated cancer-driving genes. In the present study, we investigate BRUNOL5 oncogenic functions and the role of two stilbenoids, resveratrol (RSV) and pterostilbene (PTS), in BRUNOL5 transcriptional regulation. Methods Liver cancer cells, HepG2 and SkHep1, were treated with 15µM RSV or 10µM PTS for 9 days followed by the analysis of cell growth (trypan blue exclusion test), anchorage-independent growth (soft-agar assay), and invasiveness (Boyden chamber assay). The effect on BRUNOL5 promoter methylation and gene expression was assessed by pyrosequencing and QPCR, respectively. BRUNOL5 was then depleted in HepG2 cells using siRNA followed by RNA sequencing to establish gene expression profiles. Results BRUNOL5 was down-regulated by 95% in response to RSV and by 25–50% in response to PTS. This coincided with 10–15% hypermethylation of BRUNOL5 promoter. This effect on BRUNOL5 transcriptional regulation was associated with robust decrease in cell growth, anchorage independent growth and invasiveness. Interestingly, depletion of BRUNOL5 in HepG2 cells mimicked polyphenols’ anti-cancer effects. Further investigation by RNA sequencing in BRUNOL5-depleted cells established gene targets potentially regulated by BRUNOL5. We found 4,406 genes significantly differentially expressed in response to BRUNOL5 knockdown. The top downregulated genes included cancer-promoting genes such as FAIM2, AMOTL1, and MMP2; whereas tumor suppressor genes such as MT1G, CADH1, and ALDH1L1 were among genes with the highest upregulation. Conclusions Our findings demonstrate that BRUNOL5 is a novel target of stilbenoids and acts as an oncogene in liver cancer. RSV and PTS may exert their anti-cancer effects, at least partially, through BRUNOL5 downregulation. Funding Sources UBC VP Academic Award, CFI John. R. Evans Leaders Fund, and BC Knowledge Development Fund granted to BS

scholarly journals Titanium dioxide nanoparticles induce endoplasmic reticulum stress-mediated apoptotic cell death in liver cancer cells

2020 ◽  
Vol 48 (4) ◽  
pp. 030006052090365
Author(s):  
Zhiwang Li ◽  
Jingliang He ◽  
Bowei Li ◽  
Jinqian Zhang ◽  
Ke He ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endoplasmic Reticulum ◽  
Cell Growth ◽  
Liver Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Cell Cycle Distribution ◽  
Expression Levels ◽  
Liver Cancer Cells

Objective Titanium oxide (TiO2) acts as a photosensitizer in photodynamic therapy by mediating reactive oxygen species (ROS)-induced endoplasmic reticulum (ER) stress. This study aimed to investigate the effect of TiO2 on ER stress in liver cancer cells. Methods Normal human liver and human hepatocarcinoma cell lines were incubated with various concentrations of TiO2 nanotubes for 48 hours. Cell growth, apoptosis, cell cycle, and cellular ROS were detected. Expression levels of ER stress sensors (PERK and ATF6) and Bax were evaluated by western blot. The effect of TiO2 on liver cancer growth was also investigated in mice in vivo. Results TiO2 inhibited cell growth, increased apoptosis and cellular ROS levels, and arrested the cell cycle in G1 stage in liver cancer cells. TiO2 also increased PERK, ATF6, and Bax expression levels in liver cancer cells in dose-dependent manners. TiO2 had no significant effect on cell growth, apoptosis, ROS level, cell cycle distribution, or PERK, ATF6, or Bax expression in normal liver cells. TiO2 administration reduced tumor volume and increased PERK, Bax, and ATF6 expression levels in tumor tissues in vivo. Conclusions TiO2 nanoparticles increased ROS-induced ER stress and activated the PERK/ATF6/Bax axis in liver cancer cells in vitro and in vivo.

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