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An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
The physiological estrogen metabolite 2-methoxyestradiol reduces tumor growth and induces apoptosis in human solid
1Department of General, Visceral, and Transplantation Surgery, Virchow Klinikum, Humboldt Universität Berlin, Germany.
Abstract:
2-Methoxyestradiol (2-ME) is a physiological metabolite of estrogen, which is excreted with the urine. In contrast to most estrogens, tumor growth-inhibiting effects were observed. Further studies have revealed that it may be an effective anticancer compound for many tumor types. Several different mechanisms have been attributed to 2-ME. Besides a strong antiangiogenic effect on endothelial cells and tumors, there is a tubulin-inhibiting mechanism, causing cells to arrest in the G2/ M phase of the cell cycle. In other tumors, p53-dependent and p53-independent mechanisms with induction of apoptosis have been shown. The number of different tumors examined for a growth-inhibiting effect is increasing, and new mechanisms are continuously described. In vivo studies in mice, rats, and dogs show no or very little toxicity, even at high doses. Here, we discuss the antitumor activity and their mechanisms. 2-ME appears to be a new anti-tumor compound with strong potential for clinical application.
Insights
2-Methoxyestradiol (2-ME), an estrogen metabolite, shows significant tumor growth inhibition across various cancer types. Its low toxicity and multiple anticancer mechanisms suggest strong potential for clinical application.
Area of Science:
- Endocrinology
- Oncology
- Pharmacology
Background:
- 2-Methoxyestradiol (2-ME) is a natural estrogen metabolite.
- Unlike other estrogens, 2-ME exhibits potent tumor growth-inhibiting properties.
- It is excreted in urine, indicating a physiological role.
Purpose of the Study:
- To review the antitumor activity of 2-Methoxyestradiol.
- To elucidate the diverse mechanisms underlying its anticancer effects.
- To assess its potential for clinical application in cancer therapy.
Main Methods:
- Review of existing literature on 2-ME's antitumor effects.
- Analysis of studies investigating 2-ME's impact on tumor growth and cell cycle.
- Examination of in vivo toxicity studies in animal models.
Main Results:
- 2-ME demonstrates significant inhibition of tumor growth in various cancer types.
- Key mechanisms include antiangiogenesis and tubulin inhibition, leading to G2/M cell cycle arrest.
- p53-dependent and p53-independent apoptosis induction pathways are also implicated.
- In vivo studies show minimal to no toxicity, even at high doses in mice, rats, and dogs.
Conclusions:
- 2-Methoxyestradiol exhibits broad-spectrum antitumor activity.
- Its multifaceted mechanisms of action and favorable safety profile support its potential as a novel anticancer therapeutic.
- Further clinical investigation is warranted to explore its therapeutic efficacy.
