Melatonin Anticancer Effects: Review

Bella, Giuseppe Di; Mascia, Fabrizio; Gualano, L; Bella, L. Di

doi:10.3390/ijms14022410

Cited by 145 publications

(121 citation statements)

References 128 publications

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“…Although, the mechanisms underlying are not fully understood, melatonin might exert its ant-cancer role via inducing tumor cells apoptosis and anti-proliferation and anti-angiogenesis (Di Bella et al, 2013). Melatonin has been described to be involved in inhibitory influences on sex hormone levels (Cohen et al, 1978), which have been reported to be associated with cancers of breast, endometrium, ovary, prostate, and thyroid (Henderson et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Sleep Duration and Cancer Risk: a Systematic Review and Meta-analysis of Prospective Studies

Zhao¹,

Yin²,

Yang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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To assess the risk of cancers associated with sleep duration using meta-analysis of published cohort studies, we performed a comprehensive search using PubMed, Embase and Web of Science through October 2013. We combined hazard ratios (HRs) from individual studies using meta-analysis approaches. A random effect dose-response analysis was used to evaluate the relationship between sleep duration and cancer risk. Subgroup analyses and sensitivity analyses were also performed. Publication bias was evaluated using Funnel plots and Begg's test. A total of 13 cohorts from 12 studies were included in this meta-analysis, which included 723, 337 participants with 15, 156 reported cancer outcomes during a follow-up period ranging from 7.5 to 22 years. The pooled adjusted HRs were 1.06 (95% CI: 0.92, 1.23; P for heterogeneity =0.003) for short sleep duration, 0.91 (95% CI: 0.78, 1.07; P for heterogeneity <0.0001) for long sleep duration. In subgroup analyses stratified by cancer type, long duration of sleep showed an inverse relation with hormone-related cancer (HR=0.79; 95% CI: 0.65, 0.97; P for heterogeneity =0.009) and a greater risk of colorectal cancer (HR=1.29; 95% CI: 1.09, 1.52; P for heterogeneity =0.346). Further meta-analysis on dose-response relationships showed that the relative risks of cancer were 1.00 (95% CI: 0.99, 1.01; P for linear trend=0.9151) for one hour of sleep increment per day, and 1.00 (95% CI: 0.98, 1.01; P for linear trend=0.7749) for one hour of sleep increment per night. No significant dose-response relationship between sleep duration and cancer was found on non-linearity testing (P=0.5053). Our meta-analysis suggests a positive association between long sleep duration and colorectal cancer, and an inverse association with incidence of hormone related cancers like those in the breast. Studies with larger sample size, longer follow-up times, more cancer types and detailed measure of sleep duration are warranted to confirm these results.

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Section: Discussionmentioning

confidence: 99%

Sleep Duration and Cancer Risk: a Systematic Review and Meta-analysis of Prospective Studies

Zhao¹,

Yin²,

Yang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…For example, Ramos cells (human Burkitt's lymphoma B cells) are very sensitive to melatonin caused by a dose-dependent G1-phase cell cycle arrest and apoptosis. On the other hand, melatonin in MCF-7 cells induces a delay in the progression of cell cycle, which is largely mediated through the involvement of the TGF-β pathway (Di Bella et al 2013;Sánchez-Hidalgo et al 2012;Cucina et al 2009). In addition to apoptosis, melatonin can induce other cell death pathways in cancerous cells, including autophagy and senescence (Hong et al 2014).…”

Section: Induction Of Apoptosismentioning

confidence: 99%

The melatonin immunomodulatory actions in radiotherapy

et al. 2017

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Radiotherapy has a key role in cancer treatment in more than half of patients with cancer. The management of severe side effects of this treatment modality is a limiting factor to appropriate treatment. Immune system responses play a pivotal role in many of the early and late side effects of radiation. Moreover, immune cells have a significant role in tumor response to radiotherapy, such as angiogenesis and tumor growth. Melatonin as a potent antioxidant has shown appropriate immune regulatory properties that may ameliorate toxicity induced by radiation in various organs. These effects are mediated through various modulatory effects of melatonin in different levels of tissue reaction to ionizing radiation. The effects on the DNA repair system, antioxidant enzymes, immune cells, cytokines secretion, transcription factors, and protein kinases are most important. Moreover, anti-cancer properties of melatonin may increase the therapeutic ratio of radiotherapy. Clinical applications of this agent for the management of malignancies such as breast cancer have shown promising results. It seems anti-proliferative, anti-angiogenesis, and stimulation or suppression of some immune cell responses are the main anti-tumor effects of melatonin that may help to improve response of the tumor to radiotherapy. In this review, the effects of melatonin on the modulation of immune responses in both normal and tumor tissues will be discussed.

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“…This hormone exerts oncostatic activity through a variety of mechanisms, including antiproliferative actions, anticancer immunity stimulation, modulation of expression of oncogenes, antiinflammatory, antioxidant, antiangiogenic and antimetastatic effects (20).…”

Section: Introductionmentioning

confidence: 99%

Effects of melatonin on HIF-1α and VEGF expression and on the invasive properties of hepatocarcinoma cells

et al. 2016

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Abstract. Liver cancer is the sixth most commonly occurring cancer globally, and the main histological type is hepatocellular carcinoma. This type of neoplasia has a poor prognosis due to a high rate of recurrence and intrahepatic metastasis, which are closely are closely associated with the angiogenic process. Vascular endothelial growth factor (VEGF), which is under the control of hypoxia inducible factor-1α (HIF-1α), stimulates the proliferation of endothelial cells and increases cell permeability, promoting the growth, spread and metastasis of tumors. Melatonin, the main hormone secreted by the pineal gland, may have a significant role in tumor suppression and has demonstrated antiangiogenic and antimetastatic effects. The aim of the present study was to analyze the cell viability, migration and invasion, as well as the expression of proangiogenic proteins VEGF and HIF-1α, in HepG2 hepatocarcinoma cells, following treatment with melatonin. Cells were cultured and cell viability was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of proangiogenic proteins VEGF and HIF-1α, under conditions of normoxia and hypoxia, was verified using immunocytochemistry and quantified by densitometry. The analysis of the processes of cell migration and invasion was performed in a Boyden chamber. The MTT assay revealed a reduction in cell viability (P=0.018) following treatment with 1 mM melatonin for 24 h. The expression of proangiogenic proteins VEGF and HIF-1α was reduced in cells treated with 1 mM melatonin for 24 h in normoxic (P<0.001) and hypoxic (P<0.001) conditions, compared with the control group and with induced hypoxia alone. The rate of cell migration and invasion was additionally reduced in cells treated with 1 mM melatonin for 48 h when compared with the control group (P=0.496). The results of the present study suggest that melatonin may have an antiproliferative, antiangiogenic and antimetastatic role in hepatocarcinoma cells and may present a novel therapeutic option for the treatment of liver cancer.

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Melatonin Anticancer Effects: Review

Cited by 145 publications

References 128 publications

Sleep Duration and Cancer Risk: a Systematic Review and Meta-analysis of Prospective Studies

Sleep Duration and Cancer Risk: a Systematic Review and Meta-analysis of Prospective Studies

The melatonin immunomodulatory actions in radiotherapy

Effects of melatonin on HIF-1α and VEGF expression and on the invasive properties of hepatocarcinoma cells

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