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Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting Enzymes of the Glycolytic Pathway

Propolis is rich in flavonoids and has excellent antitumor activity. However, little is known about the potential effects of propolis on glycolysis in tumor cells. Here, the antitumor effects of propolis against human breast cancer MDA-MB-231 cells in an inflammatory microenvironment stimulated with...

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Autores principales: Li, Junya, Liu, Hui, Liu, Xinying, Hao, Shengyu, Zhang, Zihan, Xuan, Hongzhuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7899755/
https://www.ncbi.nlm.nih.gov/pubmed/33628847
http://dx.doi.org/10.1155/2021/6641341
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author Li, Junya
Liu, Hui
Liu, Xinying
Hao, Shengyu
Zhang, Zihan
Xuan, Hongzhuan
author_facet Li, Junya
Liu, Hui
Liu, Xinying
Hao, Shengyu
Zhang, Zihan
Xuan, Hongzhuan
author_sort Li, Junya
collection PubMed
description Propolis is rich in flavonoids and has excellent antitumor activity. However, little is known about the potential effects of propolis on glycolysis in tumor cells. Here, the antitumor effects of propolis against human breast cancer MDA-MB-231 cells in an inflammatory microenvironment stimulated with lipopolysaccharide (LPS) were investigated by assessing the key enzymes of glycolysis. Propolis treatment obviously inhibited MDA-MB-231 cell proliferation, migration and invasion, clone forming, and angiogenesis. Proinflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6, as well as NLRP3 inflammasomes, were decreased following propolis treatment when compared with the LPS group. Moreover, propolis treatment significantly downregulated the levels of key enzymes of glycolysis–hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase muscle isozyme M2 (PKM2), and lactate dehydrogenase A (LDHA) in MDA-MB-231 cells stimulated with LPS. After treatment with 2-deoxy-D-glucose (2-DG), an inhibitor of glycolysis, the inhibitory effect of propolis on migration was not significant when compared with the LPS group. In addition, propolis increased reactive oxygen species (ROS) levels and decreased mitochondrial membrane potential. Taken together, these results indicated that propolis targeted key enzymes of glycolysis to suppress the proliferation of MDA-MB-231 cells in an inflammatory microenvironment. These studies provide a molecular basis for propolis as a natural anticancer agent against breast cancer.
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spelling pubmed-78997552021-02-23 Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting Enzymes of the Glycolytic Pathway Li, Junya Liu, Hui Liu, Xinying Hao, Shengyu Zhang, Zihan Xuan, Hongzhuan J Immunol Res Research Article Propolis is rich in flavonoids and has excellent antitumor activity. However, little is known about the potential effects of propolis on glycolysis in tumor cells. Here, the antitumor effects of propolis against human breast cancer MDA-MB-231 cells in an inflammatory microenvironment stimulated with lipopolysaccharide (LPS) were investigated by assessing the key enzymes of glycolysis. Propolis treatment obviously inhibited MDA-MB-231 cell proliferation, migration and invasion, clone forming, and angiogenesis. Proinflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6, as well as NLRP3 inflammasomes, were decreased following propolis treatment when compared with the LPS group. Moreover, propolis treatment significantly downregulated the levels of key enzymes of glycolysis–hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase muscle isozyme M2 (PKM2), and lactate dehydrogenase A (LDHA) in MDA-MB-231 cells stimulated with LPS. After treatment with 2-deoxy-D-glucose (2-DG), an inhibitor of glycolysis, the inhibitory effect of propolis on migration was not significant when compared with the LPS group. In addition, propolis increased reactive oxygen species (ROS) levels and decreased mitochondrial membrane potential. Taken together, these results indicated that propolis targeted key enzymes of glycolysis to suppress the proliferation of MDA-MB-231 cells in an inflammatory microenvironment. These studies provide a molecular basis for propolis as a natural anticancer agent against breast cancer. Hindawi 2021-02-15 /pmc/articles/PMC7899755/ /pubmed/33628847 http://dx.doi.org/10.1155/2021/6641341 Text en Copyright © 2021 Junya Li et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Li, Junya
Liu, Hui
Liu, Xinying
Hao, Shengyu
Zhang, Zihan
Xuan, Hongzhuan
Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting Enzymes of the Glycolytic Pathway
title Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting Enzymes of the Glycolytic Pathway
title_full Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting Enzymes of the Glycolytic Pathway
title_fullStr Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting Enzymes of the Glycolytic Pathway
title_full_unstemmed Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting Enzymes of the Glycolytic Pathway
title_short Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting Enzymes of the Glycolytic Pathway
title_sort chinese poplar propolis inhibits mda-mb-231 cell proliferation in an inflammatory microenvironment by targeting enzymes of the glycolytic pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7899755/
https://www.ncbi.nlm.nih.gov/pubmed/33628847
http://dx.doi.org/10.1155/2021/6641341
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