Related Experiment Video
Updated: Aug 5, 2026
Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
Suppressing M2 Macrophage Polarization by Glycine Combined with β-Elemene via the IL-6/JAK2/STAT3 Signaling Pathway
Huan Li1, Yu Cheng1, Yanyun Meng2
1Department of Traditional Chinese Medicine, Affiliated Hospital of Guizhou Medical University, Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Background:
Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis, closely associated with an imbalanced tumor immune microenvironment. Tumor-associated macrophages (TAMs) play a crucial role in tumor progression.
Purpose:
This study aimed to investigate whether glycine combined with β-elemene inhibits TNBC progression by suppressing M2 macrophage polarization through the IL-6/JAK2/STAT3 pathway.
Methods:
UPLC-Q-Exactive HRMS was used to identify glycine and β-elemene. In vitro, 4T1 cell viability was determined by CCK-8 assay. RAW264.7 cells were polarized to M2 macrophages and co-cultured with 4T1 cells. Colony formation, wound healing, and Transwell assays were performed. Western blot and immunohistochemistry were used to detect protein expression. In vitro experiments were performed with at least three independent biological replicates. In vivo, 4T1 xenograft mouse models were established (n=10 per group) to evaluate anti-tumor efficacy.
Results:
Glycine combined with β-elemene significantly suppressed proliferation, colony formation, and migration of 4T1 cells. Mechanistically, the combination inhibited M2 macrophage polarization by downregulating IL-6, p-JAK2, and p-STAT3. In vivo, the combination with paclitaxel showed the strongest anti-tumor effect, with reduced tumor volume and weight, decreased Ki-67 expression, and suppressed M2 polarization.
Conclusion:
Glycine combined with β-elemene inhibits M2 macrophage polarization by suppressing the IL-6/JAK2/STAT3 pathway, thereby exerting anti-TNBC effects. Its combination with paclitaxel demonstrates synergistic anti-tumor efficacy.
Insights
Glycine and β-elemene inhibit triple-negative breast cancer (TNBC) by suppressing M2 macrophage polarization via the IL-6/JAK2/STAT3 pathway. Combining this with paclitaxel enhances anti-tumor effects.
Area of Science:
- Oncology
- Immunology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) is aggressive with a poor prognosis.
- An imbalanced tumor immune microenvironment, particularly tumor-associated macrophages (TAMs), drives TNBC progression.
Purpose of the Study:
- To investigate the combined effect of glycine and β-elemene on TNBC.
- To determine if this combination suppresses M2 macrophage polarization via the IL-6/JAK2/STAT3 pathway.
Main Methods:
- In vitro: Assessed 4T1 cell viability, proliferation, migration, and M2 macrophage polarization.
- In vivo: Utilized 4T1 xenograft mouse models to evaluate anti-tumor efficacy.
- Detected protein expression using Western blot and immunohistochemistry.
Main Results:
- Glycine and β-elemene suppressed 4T1 cell proliferation and migration.
- The combination downregulated IL-6, p-JAK2, and p-STAT3, inhibiting M2 macrophage polarization.
- Combined with paclitaxel, it demonstrated significant anti-tumor effects in vivo, reducing tumor growth and M2 polarization.
Conclusions:
- Glycine and β-elemene inhibit M2 macrophage polarization through the IL-6/JAK2/STAT3 pathway, offering anti-TNBC effects.
- Combination therapy with paclitaxel shows synergistic anti-tumor efficacy.