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Chinese Poplar Propolis Inhibits MDA-MB-231 Cell Proliferation in an Inflammatory Microenvironment by Targeting
Junya Li1, Hui Liu1, Xinying Liu2
1School of Life Science, Liaocheng University, Liaocheng 252059, China.
Abstract:
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.
Insights
Propolis, rich in flavonoids, inhibits breast cancer cell growth by targeting glycolysis key enzymes. This natural agent reduces inflammation and tumor progression in an inflammatory environment.
Area of Science:
- Biochemistry
- Oncology
- Natural Products Chemistry
Background:
- Propolis, a natural resin, possesses known antitumor properties.
- The impact of propolis on cancer cell glycolysis, especially in inflammatory conditions, remains under-explored.
Purpose of the Study:
- To investigate the antitumor effects of propolis on human breast cancer MDA-MB-231 cells within an inflammatory microenvironment.
- To elucidate the role of propolis in modulating key glycolytic enzymes and inflammatory pathways in cancer cells.
Main Methods:
- Assessed propolis's impact on MDA-MB-231 cell proliferation, migration, invasion, clone formation, and angiogenesis.
- Measured levels of proinflammatory mediators (TNF-α, IL-1β, IL-6) and NLRP3 inflammasomes.
- Quantified key glycolytic enzymes: hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA).
- Utilized 2-deoxy-D-glucose (2-DG) to assess glycolysis inhibition and measured reactive oxygen species (ROS) and mitochondrial membrane potential.
Main Results:
- Propolis significantly inhibited MDA-MB-231 cell proliferation, migration, invasion, clone formation, and angiogenesis.
- Propolis treatment reduced levels of TNF-α, IL-1β, IL-6, and NLRP3 inflammasomes.
- Propolis downregulated key glycolytic enzymes (HK2, PFK, PKM2, LDHA) and increased ROS, decreasing mitochondrial membrane potential.
- Inhibition of glycolysis by 2-DG diminished propolis's effect on cell migration.
Conclusions:
- Propolis exhibits significant antitumor activity against breast cancer cells in an inflammatory setting.
- Propolis targets key enzymes in the glycolysis pathway to suppress cancer cell proliferation and related processes.
- These findings support propolis's potential as a natural anticancer agent for breast cancer treatment.
