Melatonin, chemotherapy, and altered gene expression in cancer

Abstract

Melatonin is a hormone synthesized and released by the pineal gland following a circadian rhythm, with low levels during the day and elevated levels at night. This indoleamine mitigates cancer at the initiation, progression and metastasis phases. Some of the anticancer actions depend of two melatonin high-affinity G protein-coupled receptors, termed MT1 and MT2, while others are receptor independent involving direct intracellular actions. Initially, most of the experiments demonstrating the oncostatic role of melatonin were conducted in hormone-dependent tumors, mainly in breast cancer. However, there is growing evidence confirming that most kinds of cancer are susceptible of inhibition by the pineal hormone. The main goal of this work is to summarize the state of the art in a review of recent studies in which melatonin has been tested, either alone, or in combination with chemotherapeutic drugs on several types such as ovary, prostate, gastric, colorectal, pancreatic, hepatic and lung cancer, leukemia and glioblastoma. Many studies have shown that melatonin’s co-administration improves the sensitivity of cancers to inhibition by conventional drugs, renders cancers previously totally resistant to treatment sensitive to these same therapies and reduces the toxic consequences of anti-cancer drugs while increasing their efficacy, contributing to the wellbeing of patients.