scholarly journals Role of Hydrogen Peroxide in the Inhibitory Effect of Ascorbate on Cell Growth.

1994 ◽  
Vol 40 (3) ◽  
pp. 219-227 ◽  
Author(s):  
Nobuhiko ARAKAWA ◽  
Shino NEMOTO ◽  
Emiko SUZUKI ◽  
Megumi OTSUKA
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Growth ◽  
Inhibitory Effect

scholarly journals Role of Apoplastic Ascorbate and Hydrogen Peroxide in the Control of Cell Growth in Pine Hypocotyls

2004 ◽  
Vol 45 (5) ◽  
pp. 530-534 ◽  
Author(s):  
Jorge Pedreira ◽  
Noelia Sanz ◽  
María Jesús Peña ◽  
María Sánchez ◽  
Eva Queijeiro ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Growth

scholarly journals THE RELATIONSHIP OF HYDROGEN PEROXIDE TO THE INHIBITION OF THE GLYOXALASE ACTIVITY OF INTACT ERYTHROCYTES BY X-RADIATION

1958 ◽  
Vol 41 (4) ◽  
pp. 737-753 ◽  
Author(s):  
S. J. Klebanoff
Keyword(s):  
Hydrogen Peroxide ◽  
Plasma Glucose ◽  
Physiological Saline ◽  
Inhibitory Effect ◽  
Enzyme Systems ◽  
Low Concentrations ◽  
X Irradiation ◽  
Ionizing Radiations ◽  
Relationship Of

The x-irradiation of a dilute suspension of erythrocytes results in a decrease in the glyoxalase activity of the cells as a result of a fall in the reduced glutathione level. The present paper deals with the possible role of H2O2 in this reaction. The addition of intact erythrocytes to physiological saline previously irradiated with 150,000 r or 225,000 r results in a fall in the glyoxalase activity of the cells. The inhibition is prevented by the preincubation of the irradiated saline with catalase and is reversed by the addition of plasma, glucose, adenosine, and inosine to the cell suspension. An inhibition of the glyoxalase activity is also produced by the addition of H2O2 to the suspension of erythrocytes. The inhibitory effect of H2O2 can be prevented and largely reversed by plasma, glucose, adenosine, and inosine. Methylglyoxal is also protective under these conditions. Hydrogen peroxide formed continuously and in low concentrations by enzyme systems appears to be more effective than added H2O2 in inhibiting the glyoxalase system. The inhibition by H2O2-producing enzyme systems is minimized by the addition of catalase, plasma, glucose, methylglyoxal, and to a lesser extent, by adenosine and inosine, and is accentuated by the addition of sodium azide. The results are discussed in relation to the role of H2O2 and catalase in the toxicity of ionizing radiations.

scholarly journals LINC00174 Facilitates Cell Proliferation, Cell Migration and Tumor Growth of Osteosarcoma via Regulating the TGF-β/SMAD Signaling Pathway and Upregulating SSH2 Expression

2021 ◽  
Vol 8 ◽  
Author(s):  
Changjun Zheng ◽  
Ronghang Li ◽  
Shuang Zheng ◽  
Hongjuan Fang ◽  
Meng Xu ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Growth ◽  
Inhibitory Effect ◽  
Loss Of Function ◽  
Protein Coding ◽  
Smad Pathway ◽  
Smad Signaling Pathway ◽  
Protein Phosphatase 2

Osteosarcoma (OS), a frequent malignant tumor which mainly occurs in the bone. The roles of long noncoding RNAs (lncRNAs) have been revealed in cancers, including OS. LncRNA long intergenic non-protein coding RNA (LINC00174) has been validated as an oncogene in several cancers. However, the role of LINC00174 in OS has not been explored. In our research, loss-of-function assays were conducted to explore the function of LINC00174 in OS cells. Then, we explored the downstream pathway of LINC00174 in OS cells. Bioinformatics, RNA pull-down and RIP experiments investigated the downstream mechanism of LINC00174 in OS cells. Finally, in vivo assays clarified the effect of LINC00174 on tumorigenesis. We found that LINC00174 was upregulated in OS tissues and cells. LINC00174 knockdown repressed OS cell growth. Mechanistically, LINC00174 knockdown suppressed the TGF-β/SMAD pathway. LINC00174 interacted with miR-378a-3p, and slingshot protein phosphatase 2 (SSH2) 3′UTR was targeted by miR-378a-3p in OS cells. Rescue assays showed that SSH2 upregulation or miR-378a-3p inhibition counteracted the inhibitory effect of LINC00174 depletion in OS cell growth. Additionally, LINC00174 depletion suppressed tumor growth in mice. In conclusion, LINC00174 promotes OS cellular malignancy and tumorigenesis via the miR-378a-3p/SSH2 axis and the TGF-β/SMAD pathway, which might provide a novel insight for OS treatment.

scholarly journals Inhibitory effect of retinol acetate on horseradish peroxidase

2013 ◽  
Vol 67 (3) ◽  
pp. 419-426
Author(s):  
Vladan Djuric ◽  
Nebojsa Deletic ◽  
Vesna Stankov-Jovanovic ◽  
Ranko Simonovic
Keyword(s):  
Hydrogen Peroxide ◽  
Horseradish Peroxidase ◽  
Enzymatic Reaction ◽  
Inhibitory Effect ◽  
Enzyme Concentration ◽  
Water Soluble ◽  
Primary Role ◽  
Retinol Acetate ◽  
Peroxidase Enzyme

Primary role of peroxidase enzyme is to decompose endogenous hydrogen peroxide, when oxygen radical is being replaced by a less potent radical, which is its cosubstrates oxidized form. During this study, catalytic activity of horseradish peroxidase has been observed in the presence of antioxidants from vitamin group, such as C, E and A, i.e. their water-soluble forms. It was found that vitamin E showed no effect on the enzyme activity and fate of cosubstrate radicals from the group of benzidine derivatives. Vitamin C proceeds enzymatic reaction showing its antioxidative character, and absorbs electrons from radicals, bringing cosubstrate back to its relaxed state. On the other hand, vitamin A plays a role of uncompetitive peroxidase inhibitor, which is visible through decreasing initial rate of catalytic reaction, and is reflected as virtual decrease of enzyme concentration. Furthermore, it prolongs life of endogenous hydrogen peroxide, which could potentially lead to oxidative stress of cells. This inhibitory effect can be used in analytical purpose, for determination of retinol acetate content in a sample.

Role of acetylcholinesterase (AChE) secreted by parasitic nematodes on the growth of the cell line from epithelial origin HT29-D4

Parasitology ◽  
1999 ◽  
Vol 118 (5) ◽  
pp. 489-498 ◽  
Author(s):  
F. HUBY ◽  
S. MALLET ◽  
H. HOSTE
Keyword(s):  
Cell Growth ◽  
Cell Line ◽  
Polyclonal Antibodies ◽  
Polyacrylamide Gel Electrophoresis ◽  
Biological Significance ◽  
Inhibitory Effect ◽  
Parasitic Nematodes ◽  
Epithelial Origin

The excretory–secretory (E–S) products of the parasitic nematodes Trichostrongylus colubriformis and Nematodirus battus were found to modify the in vitro proliferation of the tumorous colic HT29-D4 cell line of epithelial origin. A characteristic feature of these E–S products is the presence of a high level of acetylcholinesterase (AChE) activity, the biological significance of which remains unclear. To determine a possible role of AChE on cell growth, the enzyme was purified from E–S products using edrophonium chloride. Purity was confirmed by polyacrylamide gel electrophoresis, using silver and Karnovsky stains, before assessing its effects on cell proliferation. The purified AChE was incorporated at different concentrations in a culture medium of HT29-D4 cells. A mitogenic effect was shown for low concentrations (0·1–14 units). By contrast, an inhibitory effect was noted at high concentrations (35–1400 units). Furthermore, polyclonal antibodies were prepared and depletion of AChE in E–S products by immunoprecipitation or affinity chromatography resulted in a partial or total disappearance of the stimulatory effect of cell growth. Thus, the results from this in vitro study suggest a modulatory role for AChE secreted by nematode parasites on the proliferation of epithelial cells of the host.

scholarly journals A proteolytic fragment of Mcl-1 exhibits nuclear localization and regulates cell growth by interaction with Cdk1

2005 ◽  
Vol 387 (3) ◽  
pp. 659-667 ◽  
Author(s):  
Sarwat JAMIL ◽  
Rafat SOBOUTI ◽  
Payman HOJABRPOUR ◽  
Meera RAJ ◽  
Juergen KAST ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Kinase Activity ◽  
Regulatory Protein ◽  
Myeloid Cell ◽  
Cyclin B1 ◽  
Inhibitory Effect ◽  
Cell Leukaemia ◽  
Proteolytic Fragment

Mcl-1 (myeloid cell leukaemia-1) is a Bcl-2 family member with short-term pro-survival functions but whose other functions, demonstrated by embryonic lethality of knockout mice, do not involve apoptosis. In the present study, we show a cell-cycle-regulatory role of Mcl-1 involving a shortened form of the Mcl-1 polypeptide, primarily localized to the nucleus, which we call snMcl-1. snMcl-1 interacts with the cell-cycle-regulatory protein Cdk1 (cyclin-dependent kinase 1; also known as cdc2) in the nucleus, and Cdk1 bound to snMcl-1 was found to have a lower kinase activity. The interaction with Cdk1 occurs in the absence of its cyclin partners and is enhanced on treatment of cells with G2/M blocking agents, but not by G1/S blocking. The snMcl-1 polypeptide is present during S and G2 phases and is negligible in G1. Overexpression of human Mcl-1 in a murine myeloid progenitor cell line resulted in a lower rate of proliferation. Furthermore, Mcl-1-overexpressing cells had lower total Cdk1 kinase activity compared with parental cells, in both anti-Cdk1 and anti-cyclin B1 immunoprecipitates. The latter results suggest that binding to snMcl-1 alters the ability of Cdk1 to bind its conventional partner, cyclin B1. Given the important role of Cdk1 in progression through G2 and M phases, it is probable that the inhibition of Cdk1 activity accounts for the inhibitory effect of Mcl-1 on cell growth.

scholarly journals Role of Androgens on MCF-7 Breast Cancer Cell Growth and on the Inhibitory Effect of Letrozole

2006 ◽  
Vol 66 (15) ◽  
pp. 7775-7782 ◽  
Author(s):  
Luciana F. Macedo ◽  
Zhiyong Guo ◽  
Syreeta L. Tilghman ◽  
Gauri J. Sabnis ◽  
Yun Qiu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Inhibitory Effect ◽  
Cancer Cell Growth ◽  
Breast Cancer Cell Growth ◽  
Mcf 7

scholarly journals Targeting Myeloma Cell Metabolism Via Disruption of the Lnc-17-92 Transcriptional Program: Druggable New Vulnerability in Multiple Myeloma

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 317-317
Author(s):  
Eugenio Morelli ◽  
Mariateresa Fulciniti ◽  
Mehmet Kemal Samur ◽  
Caroline Ribeiro ◽  
Leon Wert-Lamas ◽  
...  
Keyword(s):  
Cell Growth ◽  
Transcriptional Control ◽  
De Novo ◽  
Cell Metabolism ◽  
Inhibitory Effect ◽  
Advisory Board ◽  
De Novo Lipogenesis

Long noncoding RNAs (lncRNA) are major regulators of chromatin dynamics and gene expression. We have recently performed deep RNA sequencing of CD138+ cells from 360 uniformly-treated, newly-diagnosed multiple myeloma (MM) patients (IFM/DFCI 2009) and described the lncRNA landscape and their role as independent risk predictors for clinical outcome in MM. Moreover, we have identified one of these lncRNAs - lnc-17-92 - as an independent risk predictor highly correlating with EFS and OS in newly-diagnosed MM providing rationale to define its molecular role in MM. Lnc-17-92 is generated at MIR17HG gene locus and is known for being involved in the biogenesis of miR-17-92 cluster of microRNAs. We here establish, for the first time, role of this transcript as a lncRNA with microRNA-independent function and molecular and biological implications in MM. Having confirmed its expression in MM cell lines and primary MM cells, we have utilized antisense oligonucleotides (n=3) to suppress lnc-17-92 expression in large panel of human MM cell lines (HMCLs) (n=12) and primary patient MM cells (n=13). Lnc-17-92 inhibition impaired MM cell proliferation leading to apoptotic cell death. This inhibitory effect was not rescued by ectopic expression of miR-17-92 microRNAs, confirming independent activity of lnc-17-92 on MM cell growth and viability. The microRNA-independent role of lnc-17-92 in transcriptional control was further confirmed using DROSHAKOcells. Analysis of transcriptomic changes after lnc-17-92 modulation in HMCLs and primary MM cells identified bona fide transcriptional targets of lnc-17-92. Using two independent MM RNA-seq datasets, we observed high correlation (R> 0.4) between lnc-17-92 expression and the expression of 12 of the transcriptional targets identified above. Interestingly, these genes were significantly enriched within metabolic pathways, suggesting an unexplored role for lnc-17-92 in MM cell metabolism. Further analysis using an RNAi-based loss-of-function screening in 3 HMCLs revealed Acetyl-CoA Carboxylase Alpha (ACC1) as a novel myeloma vulnerability. ACC1 encodes the limiting enzyme in the de novo lipogenesis pathway. Analysis of incorporation of C14-radiolabeled glucose into lipids in MM cells revealed that inhibition of ACC1 or lnc-17-92 strongly inhibited de novo lipogenesis in HMCLs and in primary MM cells. We have used ACC1 conditional KD MM cells expressing IPTG-inducible ACC1 shRNAs and confirmed significant role of ACC1 in MM cell growth and survival, both in vitro and in vivo in SCID mice model. Importantly, supplementation of palmitate, the main downstream product of ACC1 activity, significantly reverses the growth inhibitory effect of either ACC1 or lnc-17-92 suppression in MM cells. These data suggest an important role for lipogenesis pathway on lnc-17-92-promoted MM cell growth. We have further investigated mechanism by which lnc-17-92 may exert its transcriptional control. Protein-RNA pulldown assay established MYC as interacting partner of lnc-17-92. This interaction was confirmed by immunoprecipitation of MYC-bound RNA followed by qRT-PCR with specific primers for detection of lnc-17-92. ChIP-seq analysis revealed a direct binding of MYC at regulatory regions of ACC1 in MM.1S cells; these data were corroborated by the decreased ACC1 expression observed in MYC KD MM cells. Taken together, these data suggest that lnc-17-92 may function as a scaffold between MYC and the E-box motifs present on ACC1 intronic sequences, facilitating MYC binding and its transcriptional activity on ACC1. Finally, for translational application, we have pre-clinically investigated ND-646, a clinically applicable small molecule inhibitor of ACC1. Analysis of incorporation of C14-radiolabeled glucose into lipids confirmed its effect on lipogenesis in MM, which was associated with a significant in vitro growth inhibitory activity in large panel of HMCLs and primary patient MM cells. In vivo studies in murine model of human MM, using this oral agent, are ongoing and will be presented. In conclusion, we here report for the first time the microRNA-independent role of lnc-17-92 in MM pathobiology with direct impact on transcriptional control of lipogenesis. The availability of oral inhibitor of this pathway may allow the clinical application of this unique targeted therapy in MM. Disclosures Anderson: Janssen: Other: Advisory Board; Gilead Sciences: Other: Advisory Board; OncoPep: Other: Scientific founder ; Sanofi-Aventis: Other: Advisory Board; C4 Therapeutics: Other: Scientific founder . Munshi:Abbvie: Consultancy; Adaptive: Consultancy; Amgen: Consultancy; Celgene: Consultancy; Janssen: Consultancy; Adaptive: Consultancy; Oncopep: Consultancy; Celgene: Consultancy; Takeda: Consultancy; Janssen: Consultancy; Oncopep: Consultancy; Takeda: Consultancy; Amgen: Consultancy; Abbvie: Consultancy.

scholarly journals Inhibitory effect of adiponectin on breast cancer cell growth: evidences of the crucial role of ERα expression

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Loredana Mauro ◽  
Michele Pellegrino ◽  
Francesca De Amicis ◽  
Cinzia Giordano ◽  
Sebastiano Andò
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Crucial Role ◽  
Inhibitory Effect ◽  
Cancer Cell Growth ◽  
Breast Cancer Cell Growth
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