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Targeting Breast Cancer with N-Acetyl-D-Glucosamine: Integrating Machine Learning and Cellular Assays for Promising
Ömür Baysal1, Deniz Genç2, Ragıp Soner Silme3
1Department of Molecular Biology and Genetics, Faculty of Science, Molecular Microbiology Unit, Muğla Sıtkı Koçman University, Kötekli-Muğla, Türkiye.
Background:
Breast cancer is a common cancer with high mortality rates. Early diagnosis is crucial for reducing the prognosis and mortality rates. Therefore, the development of alternative treatment options is necessary.
Objective:
This study aimed to investigate the inhibitory effect of N-acetyl-D-glucosamine (D-GlcNAc) on breast cancer using a machine learning method. The findings were further confirmed through assays on breast cancer cell lines.
Methods:
MCF-7 and 4T1 cell lines (ATCC) were cultured in the presence and absence of varying concentrations of D-GlcNAc (0.5 mM, 1 mM, 2 mM, and 4 mM) for 72 hours. A xenograft mouse model for breast cancer was established by injecting 4T1 cells into mammary glands. D-GlcNAc (2 mM) was administered intraperitoneally to mice daily for 28 days, and histopathological effects were evaluated at pre-tumoral and post-tumoral stages.
Results:
Treatment with 2 mM and 4 mM D-GlcNAc significantly decreased cell proliferation rates in MCF-7 and 4T1 cell lines and increased Fas expression. The number of apoptotic cells was significantly higher than untreated cell cultures (p < 0.01 - p < 0.0001). D-GlcNAc administration also considerably reduced tumour size, mitosis, and angiogenesis in the post-treatment group compared to the control breast cancer group (p < 0.01 - p < 0.0001). Additionally, molecular docking/dynamic analysis revealed a high binding affinity of D-GlcNAc to the marker protein HER2, which is involved in tumour progression and cell signalling.
Conclusion:
Our study demonstrated the positive effect of D-GlcNAc administration on breast cancer cells, leading to increased apoptosis and Fas expression in the malignant phenotype. The binding affinity of D-GlcNAc to HER2 suggests a potential mechanism of action. These findings contribute to understanding D-GlcNAc as a potential anti-tumour agent for breast cancer treatment.
Insights
N-acetyl-D-glucosamine (D-GlcNAc) shows promise as a breast cancer treatment, significantly increasing cancer cell apoptosis and reducing tumor growth. Its high binding affinity to HER2 suggests a potential therapeutic mechanism for breast cancer.
Area of Science:
- Biochemistry
- Oncology
- Computational Biology
Background:
- Breast cancer presents a significant global health challenge with high mortality rates.
- Early diagnosis and novel therapeutic strategies are crucial for improving patient outcomes.
- There is a need for alternative treatment options to combat breast cancer effectively.
Purpose of the Study:
- To investigate the potential anti-cancer effects of N-acetyl-D-glucosamine (D-GlcNAc) on breast cancer.
- To utilize machine learning and cell line assays to confirm the inhibitory effects of D-GlcNAc.
- To explore the mechanism of action of D-GlcNAc in breast cancer treatment.
Main Methods:
- Cultured MCF-7 and 4T1 breast cancer cell lines with varying concentrations of D-GlcNAc.
- Established a xenograft mouse model by injecting 4T1 cells and administering D-GlcNAc.
- Evaluated histopathological effects, cell proliferation, apoptosis, and molecular interactions (HER2 binding).
Main Results:
- D-GlcNAc (2 mM and 4 mM) significantly reduced breast cancer cell proliferation and increased Fas expression and apoptosis.
- In vivo studies showed D-GlcNAc reduced tumor size, mitosis, and angiogenesis.
- Molecular docking revealed a strong binding affinity of D-GlcNAc to the HER2 protein.
Conclusions:
- D-GlcNAc demonstrates a significant positive impact on breast cancer cells, enhancing apoptosis and Fas expression.
- The binding affinity to HER2 suggests a potential therapeutic pathway for D-GlcNAc in breast cancer.
- These findings support D-GlcNAc as a potential anti-cancer agent for breast cancer therapy.
