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.

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 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 Corosolic acid inhibits cancer progression by decreasing the level of CDK19-mediated O-GlcNAcylation in liver cancer cells

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Congcong Zhang ◽  
Yongjie Niu ◽  
Zhixian Wang ◽  
Xin Xu ◽  
Yan Li ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Progression ◽  
High Glucose ◽  
Antitumor Effects ◽  
Glucose Levels ◽  
Liver Cancer Cells ◽  
Corosolic Acid ◽  
Hcc Cells

AbstractDiabetes is an important risk factor for liver cancer, but its mechanism is unknown. Corosolic acid (CA) has been proven to have both hypoglycemic and antitumor effects, so revealing the function of CA can help us understand the relationship between diabetes and liver cancer. In previous studies, we confirmed that CA can effectively inhibit the expression of YAP, an important oncoprotein in HCC cells, and the proliferation of HCC cells. In addition, we also found that O-GlcNAcylation plays an indispensable role in HCC tumorigenesis. However, it is not clear whether CA can inhibit the effect of O-GlcNAcylation on HCC cells. In this study, the antitumor ability of CA was investigated by inhibiting the O-GlcNAcylation level and its corresponding mechanism. The results showed that HG (high glucose) could promote the proliferation of liver cancer cells, while CA could inhibit cell growth under HG conditions and tumor growth in a xenotransplantation model. CA can inhibit the activation of the HBP pathway and reduce the expression of YAP and OGT under HG conditions. Importantly, we found that CA can reduce YAP expression and O-GlcNAcylation by inhibiting the activity of CDK19. Overexpression of CDK19 partially reversed the CA-induced decrease in YAP and O-GlcNAcylation. This is the first evidence that CA can reduce the proliferative capacity of cells with high glucose levels and further inhibit tumor growth by inactivating the CDK19/YAP/O-GlcNAcylation pathway, suggesting that CA is a candidate drug for the development of treatments against diabetes-associated liver cancer.

scholarly journals RAB9A Plays an Oncogenic Role in Human Liver Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Pengfei Sun ◽  
Lei Li ◽  
Zhongchao Li
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Apoptotic Pathway ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Hep3b Cells ◽  
Human Liver Cancer Cells

Background. RAB9, as a member of the Rab GTPase family, is required for the transport of the mannose-6-phosphate receptor (MPR) from late endosomes to trans-Golgi network (TGN). However, the role of RAB9A in tumors, including liver cancer, is still unknown. Methods. We used pcDNA3.1 plasmid to upregulate the expression of RAB9A in Hep3b cells and used specific shRNA to downregulate the expression of RAB9A in HepG2 cells. Biological functions of RAB9A were performed by CCK-8 assay, colony formation assay, apoptosis analysis, transwell assays, and wound healing assays. Finally, an in-depth mechanism study was performed by western blot. Results. RAB9A promoted the proliferation and clonality of Hep3b and HepG2 cells. RAB9A also inhibited apoptosis and the activation of mitochondrial apoptotic pathway. In addition, RAB9A promoted the invasion and migration of Hep3b and HepG2 cells. Importantly, RAB9A activated the AKT/mTOR signaling pathway in human liver cancer cells. A double-effect inhibitor (BEZ235) significantly hindered the effect of RAB9A overexpression on the proliferation and invasion of Hep3b cells. Conclusion. Our data suggest that RAB9A plays a carcinogenic role in human liver cancer progression partially through AKT signaling pathways, suggesting that RAB9A may serve as a potential therapeutic target for liver cancer therapy.

MicroRNA-64 Promotes Progression of Liver Cancer Through Targeting X-Box Binding Protein 1 (XBP1)

2021 ◽  
Vol 11 (8) ◽  
pp. 1555-1559
Author(s):  
Haiying Jiang ◽  
Jieming Yi ◽  
Shouren Cheng
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Binding Protein ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Liver Cancer Cells ◽  
Potential Binding ◽  
Gene Assay ◽  
Insight Into

Liver cancer is still a horrible threat to people’s health worldwide. Herein, we aimed to explore the mechanism underlying microRNA (miR)-64’s role in liver cancer progression to provide novel insight into therapy. Expression of miR-64 in liver cancer cells was determined by RT-qPCR. Luciferase reporter gene assay detected the potential binding between miR-64 and X-box binding protein 1 (XBP1). Cancer cells were transfected with specific plasmids of XBP1, followed by MTT experiment and Ttranswell assay to assess invasion and proliferation. miR-64 was highly expressed in liver cancer cells and positively correlated with cell proliferation, invasion, and metastasis. miR-64 targeted and inhibited XBP1 expression. Overexpression of miR-64 significantly resulted in increased cell viability and invasion. Taken altogether, miR-64 promotes liver cancer through inhibiting XBP1, providing insight into miR-64-based targeted therapy against liver cancer.

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