scholarly journals Gallic Acid Derivatives Propyl Gallate and Epigallocatechin Gallate Reduce rRNA Transcription via Induction of KDM2A Activation

Biomolecules ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 30
Author(s):  
Yuji Tanaka ◽  
Makoto Tsuneoka
Keyword(s):  
Cell Proliferation ◽  
Gallic Acid ◽  
Cancer Cell ◽  
Propyl Gallate ◽  
Epigallocatechin Gallate ◽  
Cancer Cell Line ◽  
Rrna Gene ◽  
Ros Production ◽  
Rrna Transcription ◽  
Mcf 7

We previously reported that lysine-demethylase 2A (KDM2A), a Jumonji-C histone demethylase, is activated by gallic acid to reduce H3K36me2 levels in the rRNA gene promoter and consequently inhibit rRNA transcription and cell proliferation in the breast cancer cell line MCF-7. Gallic acid activates AMP-activated protein kinase (AMPK) and increases reactive oxygen species (ROS) production to activate KDM2A. Esters of gallic acid, propyl gallate (PG) and epigallocatechin gallate (EGCG), and other chemicals, reduce cancer cell proliferation. However, whether these compounds activate KDM2A has yet to be tested. In this study, we found that PG and EGCG decreased rRNA transcription and cell proliferation through KDM2A in MCF-7 cells. The activation of both AMPK and ROS production by PG or EGCG was required to activate KDM2A. Of note, while the elevation of ROS production by PG or EGCG was limited in time, it was sufficient to activate KDM2A. Importantly, the inhibition of rRNA transcription and cell proliferation by gallic acid, PG, or EGCG was specifically observed in MCF-7 cells, whereas it was not observed in non-tumorigenic MCF10A cells. Altogether, these results suggest that the derivatization of gallic acid may be used to obtain new compounds with anti-cancer activity.

Leccinum vulpinum Watling induces DNA damage, decreases cell proliferation and induces apoptosis on the human MCF-7 breast cancer cell line

2016 ◽  
Vol 90 ◽  
pp. 45-54 ◽  
Author(s):  
Filipa S. Reis ◽  
Diana Sousa ◽  
Lillian Barros ◽  
Anabela Martins ◽  
Patricia Morales ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Dna Damage ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Cancer Cell Line ◽  
Mcf 7

scholarly journals Mild Glucose Starvation Induces KDM2A-Mediated H3K36me2 Demethylation through AMPK To Reduce rRNA Transcription and Cell Proliferation

2015 ◽  
Vol 35 (24) ◽  
pp. 4170-4184 ◽  
Author(s):  
Yuji Tanaka ◽  
Hirohisa Yano ◽  
Sachiko Ogasawara ◽  
Sho-ichi Yoshioka ◽  
Hiromi Imamura ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Line ◽  
Breast Cancer Cell Line ◽  
Triple Negative ◽  
Cancer Cell Line ◽  
Glucose Starvation ◽  
Rrna Transcription ◽  
Cancer Tissues ◽  
Mcf 7

Environmental conditions control rRNA transcription. Previously, we found that serum and glucose deprivation induces KDM2A-mediated H3K36me2 demethylation in the rRNA gene (rDNA) promoter and reduces rRNA transcription in the human breast cancer cell line MCF-7. However, the molecular mechanism and biological significance are still unclear. In the present study, we found that glucose starvation alone induced the KDM2A-dependent reduction of rRNA transcription. The treatment of cells with 2-deoxy-d-glucose, an inhibitor of glycolysis, reduced rRNA transcription and H3K36me2 in the rDNA promoter, both of which were completely dependent on KDM2A in low concentrations of 2-deoxy-d-glucose, that is, mild starvation conditions. The mild starvation induced these KDM2A activities through AMP-activated kinase (AMPK) but did not affect another AMPK effector of rRNA transcription, TIF-IA. In the triple-negative breast cancer cell line MDA-MB-231, the mild starvation also reduced rRNA transcription in a KDM2A-dependent manner. We detected KDM2A in breast cancer tissues irrespective of their estrogen receptor, progesterone receptor, and HER2 status, including triple-negative cancer tissues. In both MCF-7 and MDA-MB-231 cells, mild starvation reduced cell proliferation, and KDM2A knockdown suppressed the reduction of cell proliferation. These results suggest that under mild glucose starvation AMPK induces KDM2A-dependent reduction of rRNA transcription to control cell proliferation.

scholarly journals Production of ROS by Gallic Acid Activates KDM2A to Reduce rRNA Transcription

Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2266
Author(s):  
Yuji Tanaka ◽  
Hideru Obinata ◽  
Akimitsu Konishi ◽  
Noriyuki Yamagiwa ◽  
Makoto Tsuneoka
Keyword(s):  
Cell Proliferation ◽  
Gallic Acid ◽  
Control Cell ◽  
Ros Production ◽  
Breast Cancers ◽  
Rrna Transcription ◽  
Anti Cancer ◽  
Ampk Activity ◽  
Mcf10a Cells ◽  
Additive Compound

Metformin, which is suggested to have anti-cancer effects, activates KDM2A to reduce rRNA transcription and proliferation of cancer cells. Thus, the specific activation of KDM2A may be applicable to the treatment of cancers. In this study, we screened a food-additive compound library to identify compounds that control cell proliferation. We found that gallic acid activated KDM2A to reduce rRNA transcription and cell proliferation in breast cancer MCF-7 cells. Gallic acid accelerated ROS production and activated AMPK. When ROS production or AMPK activity was inhibited, gallic acid did not activate KDM2A. These results suggest that both ROS production and AMPK activation are required for activation of KDM2A by gallic acid. Gallic acid did not reduce the succinate level, which was required for KDM2A activation by metformin. Metformin did not elevate ROS production. These results suggest that the activation of KDM2A by gallic acid includes mechanisms distinct from those by metformin. Therefore, signals from multiple intracellular conditions converge in KDM2A to control rRNA transcription. Gallic acid did not induce KDM2A-dependent anti-proliferation activity in non-tumorigenic MCF10A cells. These results suggest that the mechanism of KDM2A activation by gallic acid may be applicable to the treatment of breast cancers.

scholarly journals ANTIBACTERIAL AND ANTICANCER POTENTIAL OF SILVER NANOPARTICLES SYNTHESIZED USING GALLIC ACID IN BENTONITE/STARCH BIO-NANOCOMPOSITES

2018 ◽  
Vol 10 (5) ◽  
pp. 178 ◽  
Author(s):  
Anupama Thapliyal ◽  
Amrish Chandra
Keyword(s):  
Silver Nanoparticles ◽  
Zeta Potential ◽  
Gallic Acid ◽  
Cell Line ◽  
Cancer Cell ◽  
Low Cost ◽  
Cancer Cell Line ◽  
Diffusion Method ◽  
Potential Candidate ◽  
Mcf 7

Objective: To optimize and synthesize eco-friendly and low-cost silver nanoparticles (AgNPs) by using gallic acid (GA) reducing agent in bentonite/starch bio-nanocomposites (BNCs) for oral use and to evaluate its antibacterial and anticancer efficacy.Methods: An artificial neural network (ANN) model was employed for the optimization and evaluate the effect of the formulation variables on the entrapment efficiency (EE) of AgNPs. The synthesized AgNPs in BNCs were characterized using UV-vis spectroscopy, energy dispersive X-ray spectroscopy (EDXA), dynamic light scattering (DLS), scanning electron microscopy (SEM), zeta potential and fourier transform infrared spectroscopy (FTIR). Elemental ion analysis was carried out using inductively coupled plasma mass spectrometry (ICP-MS). Drug release study was carried out. The antimicrobial efficacy determined by agar well diffusion method. In vitro anticancer efficacy of AgNPs in breast cancer cell line (MCF-7) by MTT assay was performed.Results: The formation of AgNPs was confirmed by UV-vis absorbance peak shown at 412 nm. XRD spectrum has indicated the face-centered cubic structure of the synthesized AgNPs. SEM and DLS measurements showed spherical nanoparticles with a mean size of 68.06±0.2 nm. The negative surface zeta potential with-32±0.25 mV has indicated colloidal stability of nanoparticles. FTIR spectra confirmed no interaction observed between drug and excipients. AgNPs showed significant EE with 80±0.25%. The synthesized AgNPs in BNCs is a potential candidate for inhibiting the growth of pathogenic bacteria and showed significant cytotoxicity against MCF-7 cancer cell line with IC50 of 160±0.014μg/ml.Conclusion: The present research confirms that the green synthesized AgNPs in BNCs can be a promising antibacterial and anticancer agent regarding stability, low cost and easy preparation.

scholarly journals Açai (Euterpe oleracea Mart.) Seed Extract Induces ROS Production and Cell Death in MCF-7 Breast Cancer Cell Line

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3546
Author(s):  
Marcos Antonio Custódio Neto da Silva ◽  
Jonas Henrique Costa ◽  
Taícia Pacheco-Fill ◽  
Ana Lúcia Tasca Gois Ruiz ◽  
Flávia Castello Branco Vidal ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cell Line ◽  
Cancer Cell Line ◽  
Seed Extract ◽  
Ros Production ◽  
Molecular Networking ◽  
Mcf 7

Euterpe oleracea Mart. (açai) is a native palm from the Amazon region. There are various chemical constituents of açai with bioactive properties. This study aimed to evaluate the chemical composition and cytotoxic effects of açai seed extract on breast cancer cell line (MCF-7). Global Natural Products Social Molecular Networking (GNPS) was applied to identify chemical compounds present in açai seed extract. LC-MS/MS and molecular networking were employed to detect the phenolic compounds of açai. The antioxidant activity of açai seed extract was measured by DPPH assay. MCF-7 breast cancer cell line viability was evaluated by MTT assay. Cell death was evaluated by flow cytometry and time-lapse microscopy. Autophagy was evaluated by orange acridin immunofluorescence assay. Reactive oxygen species (ROS) production was evaluated by DAF assay. From the molecular networking, fifteen compounds were identified, mainly phenolic compounds. The açai seed extract showed cytotoxic effects against MCF-7, induced morphologic changes in the cell line by autophagy and increased the ROS production pathway. The present study suggests that açai seed extract has a high cytotoxic capacity and may induce autophagy by increasing ROS production in breast cancer. Apart from its antioxidant activity, flavonoids with high radical scavenging activity present in açai also generated NO (nitric oxide), contributing to its cytotoxic effect and autophagy induction.

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