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Dietary Melatonin and Glycine Decrease Tumor Growth through Antiangiogenic Activity in Experimental Colorectal Liver
Mindaugas Kvietkauskas1,2, Viktorija Zitkute1,2, Bettina Leber1
1General, Visceral and Transplant Surgery, Department of Surgery, Medical University of Graz, Auenbruggerplatz 2, 8036 Graz, Austria.
Nutrients
|July 2, 2021
Summary
Melatonin and glycine alone inhibit colorectal cancer liver metastasis growth by reducing tumor volume and proliferation. Combination therapy showed no additional benefit, but both agents exhibited antiangiogenic properties.
Area of Science:
- Oncology
- Pharmacology
- Immunology
Background:
- Advanced colorectal cancer (CRC) outcomes are poor despite multimodal treatments.
- Chemotherapy for CRC is limited by resistance, toxicity, and side effects.
- Melatonin and glycine possess anti-cancer properties with minimal side effects.
Purpose of the Study:
- To investigate the combined effects of melatonin and glycine on experimental colorectal cancer liver metastases.
- To evaluate their impact on tumor volume, proliferation, microvascular density, and immune parameters.
Main Methods:
- Experimental liver metastases were induced in Wistar rats using CC531 cells.
- Rats were supplemented with melatonin, glycine, or their combination for 14 days.
- Tumor volume, proliferation (Ki67), microvascular density (CD31), and blood parameters were analyzed.
Main Results:
- Melatonin and glycine monotherapy significantly reduced tumor volume (63.2% and 43%, respectively) and proliferation.
- Combination therapy did not yield additional benefits on tumor parameters.
- Both agents demonstrated antiangiogenic effects by reducing tumor microvascular density.
- Melatonin increased leukocyte and lymphocyte counts.
Conclusions:
- Melatonin and glycine alone show inhibitory effects on colorectal cancer liver metastasis growth.
- These compounds act as natural antiangiogenic molecules, impacting angiogenesis-dependent proliferation.
- Further research into their immunomodulatory effects is warranted.
