Effect of L-Ascorbic Acid on Leukemia Development and Breast Cancer in Various Inbred Strains of Mice1

2015 ◽  
pp. 140-143 ◽  
Author(s):  
B. Leibovitz ◽  
J. Schlesser
Keyword(s):  
Breast Cancer ◽  
Ascorbic Acid ◽  
Inbred Strains ◽  
Leukemia Development

scholarly journals Potassium increases the antitumor effects of ascorbic acid in breast cancer cell lines in vitro

2016 ◽  
Vol 11 (6) ◽  
pp. 4224-4234 ◽  
Author(s):  
GIOVANNI VANNI FRAJESE ◽  
MONICA BENVENUTO ◽  
MASSIMO FANTINI ◽  
ELENA AMBROSIN ◽  
PAMELA SACCHETTI ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ascorbic Acid ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Antitumor Effects

scholarly journals Causes and Consequences of A Glutamine Induced Normoxic HIF1 Activity for the Tumor Metabolism

2019 ◽  
Vol 20 (19) ◽  
pp. 4742 ◽  
Author(s):  
Matthias Kappler ◽  
Ulrike Pabst ◽  
Claus Weinholdt ◽  
Helge Taubert ◽  
Swetlana Rot ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ascorbic Acid ◽  
Amino Acid ◽  
Tumor Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Glutamine Metabolism ◽  
Dependent Manner ◽  
Acetyl Coa ◽  
Hypoxic Conditions

The transcription factor hypoxia-inducible factor 1 (HIF1) is the crucial regulator of genes that are involved in metabolism under hypoxic conditions, but information regarding the transcriptional activity of HIF1 in normoxic metabolism is limited. Different tumor cells were treated under normoxic and hypoxic conditions with various drugs that affect cellular metabolism. HIF1α was silenced by siRNA in normoxic/hypoxic tumor cells, before RNA sequencing and bioinformatics analyses were performed while using the breast cancer cell line MDA-MB-231 as a model. Differentially expressed genes were further analyzed and validated by qPCR, while the activity of the metabolites was determined by enzyme assays. Under normoxic conditions, HIF1 activity was significantly increased by (i) glutamine metabolism, which was associated with the release of ammonium, and it was decreased by (ii) acetylation via acetyl CoA synthetase (ACSS2) or ATP citrate lyase (ACLY), respectively, and (iii) the presence of L-ascorbic acid, citrate, or acetyl-CoA. Interestingly, acetylsalicylic acid, ibuprofen, L-ascorbic acid, and citrate each significantly destabilized HIF1α only under normoxia. The results from the deep sequence analyses indicated that, in HIF1-siRNA silenced MDA-MB-231 cells, 231 genes under normoxia and 1384 genes under hypoxia were transcriptionally significant deregulated in a HIF1-dependent manner. Focusing on glycolysis genes, it was confirmed that HIF1 significantly regulated six normoxic and 16 hypoxic glycolysis-associated gene transcripts. However, the results from the targeted metabolome analyses revealed that HIF1 activity affected neither the consumption of glucose nor the release of ammonium or lactate; however, it significantly inhibited the release of the amino acid alanine. This study comprehensively investigated, for the first time, how normoxic HIF1 is stabilized, and it analyzed the possible function of normoxic HIF1 in the transcriptome and metabolic processes of tumor cells in a breast cancer cell model. Furthermore, these data imply that HIF1 compensates for the metabolic outcomes of glutaminolysis and, subsequently, the Warburg effect might be a direct consequence of the altered amino acid metabolism in tumor cells.

In Vitro and In Vivo Antitumorigenic Activity of a Mixture of Lysine, Proline, Ascorbic Acid, and Green Tea Extract on Human Breast Cancer Lines MDA-MB-231 and MCF-7

2005 ◽  
Vol 22 (2) ◽  
pp. 129-138 ◽  
Author(s):  
M. Waheed Roomi ◽  
Vadim Ivanov ◽  
Tatiana Kalinovsky ◽  
Aleksandra Niedzwiecki ◽  
Matthias Rath
Keyword(s):  
Breast Cancer ◽  
Ascorbic Acid ◽  
Green Tea ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Antitumorigenic Activity ◽  
Tea Extract ◽  
Mcf 7

Combination Effect of Tamoxifen and Ascorbic Acid Treatment on Breast Cancer Cells (MCF-7) and Cervical Cancer Cells (HeLa)

2021 ◽  
Vol 19 (02) ◽  
pp. 99-109
Author(s):  
HASMAH ABDULLAH ◽  
NORLIDA MAMAT ◽  
NOR MUNIRAH ZAKARIA ◽  
NUR IMAN FATIHAH MOHD YUNAN ◽  
MUHAMMAD IRFAN NOOR HISHAM ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cervical Cancer ◽  
Ascorbic Acid ◽  
Cancer Cells ◽  
Acid Treatment ◽  
Breast Cancer Cells ◽  
Combination Effect ◽  
Cervical Cancer Cells ◽  
Mcf 7

Synthesis, biological evaluation and molecular docking studies against EGFR tyrosine kinase of 3,5-bis(substituted benzylidene)-1-ethylpiperidin-4-one analogues

2020 ◽  
Vol 17 ◽  
Author(s):  
Mohamed Jawed Ahsan ◽  
Deepak Saini ◽  
Piush Sharma ◽  
Surender Singh Jadav ◽  
Mohammad Afroz Bakht ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Antioxidant Activity ◽  
Ascorbic Acid ◽  
Tyrosine Kinase ◽  
Anticancer Activity ◽  
Cancer Cell Line ◽  
Docking Studies ◽  
Molecular Target ◽  
Standard Drug ◽  
Mcf 7

Background:: Cancer is one of the leading causes of death. The aim of present studies is to synthesize and investigate the anticancer and antioxidant activities of some 3,5-bis(substituted benzylidene)-1-ethylpiperidin-4-one analogues (4a-g). The 3,5-bis(substituted benzylidene)-1-ethylpiperidin-4-one analogues (4a-g) was prepared from the precursor, piperidin-4-one hydrochloride (1). The initial step involved the synthesis of intermediates, 3,5-bis(substituted benzylidene)piperidin-4-one analogues (3a-g) followed by their ethylation with C2H5I in acetone and K2CO3 to obtain the title compounds (4a-g). The Fourier transform infrared (FTIR), nuclear magnetic resonance (1H & 13C NMR), mass spectrometry and microanalysis were used to characterized the title compounds (4a-g). All the compounds were further evaluated for their anticancer activity by SRB assay and NCI US protocol, while the antioxidant activity was evaluated by DPPH free radical assay. All the title com-pounds (4a-g) were subjected to molecular docking studies against EGRF tyrosine kinase, a potential target for anticancer agents, to study the possible mode of interaction of our compounds with the molecular target. The compound, 4g showed significant anticancer activity with GI50 of 28.2 μM against MCF-7 (Breast cancer cell line). The antioxidant activity of compound, 4g (IC50 = 14.98±0.91 μM) was found to be comparable to the standard drug ascorbic acid. The binding modes of compounds, 4a-g against the molecular target EGFR tyrosine kinase were also studied. The structure activity relationship (SAR) was also studied. The compound, 4g showed significant anticancer activity with GI50 of 28.2 μM against MCF-7 (Breast cancer cell line). The antioxidant activity of the compound, 4g was found to be comparable to the standard drug ascorbic acid, while its anticancer activity was found to be less than that of the standard drug adriamycin.

vHTS and 3D-QSAR for the Identification of Novel Phyto-inhibitors of Farnesyltransferase: Validation of Ascorbic Acid inhibition of Farnesyltransferase in an Animal Model of Breast Cancer

Drug Research ◽  
2021 ◽  
Author(s):  
Damilohun Samuel Metibemu
Keyword(s):  
Breast Cancer ◽  
Animal Model ◽  
Ascorbic Acid ◽  
Curcuma Longa ◽  
Three Dimensional ◽  
3D Qsar ◽  
Qsar Model ◽  
Quantitative Structure Activity Relationship ◽  
Farnesyltransferase Inhibitors ◽  
Hydrogen Bond Interactions

AbstractFarnesyltransferase (FTase) is a zinc enzyme that has been the subject of attention in anti-cancer research over the past. In this study, phytochemicals from Curcuma longa L., Taraxacum officinale, and Spondias mombin plants were screened for their inhibitory potentials on the human farnesyltransferase. A three-dimensional quantitative structure-activity relationship (3D-QSAR) model for the inhibition of farnesyltransferase was generated and the inhibition of farnesyltransferase by the hit, ascorbic acid was validated in an animal model of breast cancer. The lead compound, ascorbic acid makes extensive hydrogen bond interactions with key residues, lys-353, tyr-300, gly-290, leu-290 within the active site of farnesyltransferase. It downregulated the expression of FNTA mRNA in an animal model of breast cancer. The 3D-QSAR generated herein is robust, thoroughly validated, and should be employed in the pipelining of novel farnesyltransferase inhibitors. Ascorbic acid demonstrates its anticancer potentials through the inhibition of farnesyltransferase.

scholarly journals L-Ascorbic Acid Inhibits Breast Cancer Growth by Inducing IRE/JNK/CHOP-Related Endoplasmic Reticulum Stress-Mediated p62/SQSTM1 Accumulation in the Nucleus

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1351 ◽  
Author(s):  
Youn Kyung Choi ◽  
Jung-Il Kang ◽  
Sanghoon Han ◽  
Young Ree Kim ◽  
Jaemin Jo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Ascorbic Acid ◽  
Er Stress ◽  
Cancer Cells ◽  
Cancer Growth ◽  
Autophagic Flux ◽  
Sequestosome 1 ◽  
Breast Cancer Growth

Anticancer effects of L-ascorbic acid (Vitamin C, L-AA) have been reported in various types of cancers. L-AA intake reduces breast cancer recurrence and mortality; however, the role of L-AA in the treatment of breast cancer remains poorly understood. In this study, we investigated the effect and mechanism action of L-AA on breast cancer growth. L-AA inhibited the growth of breast cancer cells by inducing apoptotic cell death at the evaluated treatment concentrations without affecting normal cells. Moreover, L-AA induces autophagosome formation via regulation of mammalian target of rapamycin (mTOR), Beclin1, and autophagy-related genes (ATGs) and increased autophagic flux. Notably, we observed that L-AA increased p62/SQSTM1 (sequestosome 1) protein levels. Accumulation of p62 protein in cancer cells in response to stress has been reported, but its role in cancer regulation remains controversial. Here, we demonstrated that L-AA-induced p62 accumulation is related to L-AA-induced breast cancer growth inhibition. Furthermore, L-AA induced endoplasmic reticulum (ER) stress via the IRE–JNK–CHOP (inositol-requiring endonuclease–c-Jun N-terminal kinase–C/EBP homologous protein) signaling pathways, which increased the nuclear levels of p62/SQSTM1. These findings provide evidence that L-AA-induced ER stress could be crucial for p62 accumulation-dependent cell death, and L-AA can be useful in breast cancer treatment.

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