The impact of different extracellular matrices on melatonin effect in proliferation and stemness properties of ovarian cancer cells

Akbarzadeh, Maryam; Rahbarghazi‬, Reza; Nabat, Elahe; Movassaghpour, Aliakbar; Shanehbandi, Dariush; Maragheh, Behnaz Faramarzian Azimi; Matluobi, Danial; Barazvan, Balal; Masoume, Kazemi,; Samadi, Nasser; Nouri, Mohammad

doi:10.1016/j.biopha.2016.12.119

Cited by 21 publications

(21 citation statements)

References 37 publications

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“…Melatonin is relevant in targeting CSC because they exhibit circadian rhythmicity. In accordance with the foregoing, melatonin clearly has demonstrated debilitating effects on tumor cells, but also specific oncostatic actions on subpopulations of colorectal and noncolorectal CSC. Thus, melatonin administration (10 mg/day, IP for 2 weeks) to male rats exposed to constant light and treated with the CRC carcinogen DMH, reduced the incidence of aberrant crypt foci, diminished the development of preneoplastic and dysplastic lesions in pericryptal colonic stroma, and stimulated apoptosis and, thereby, prevented CRC, probably through the control of reproduction and differentiation of CSC.…”

Section: Melatonin and P53: The “Cancer Stem Cell Hypothesis”supporting

confidence: 76%

“…250 Melatonin is relevant in targeting CSC because they exhibit circadian rhythmicity. In accordance with the foregoing, melatonin clearly has demonstrated debilitating effects on tumor cells, but also specific oncostatic actions on subpopulations of colorectal 251,252 and noncolorectal [253][254][255] CSC. Thus, melatonin administration (10 mg/day, IP for 2 weeks) to male rats exposed to constant light and treated with the CRC carcinogen DMH, reduced the incidence Figure 3).…”

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confidence: 76%

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The emergence of melatonin in oncology: Focus on colorectal cancer

Gil‐Martín

Egea

Reíter

et al. 2019

Medicinal Research Reviews

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Within the last few decades, melatonin has increasingly emerged in clinical oncology as a naturally occurring bioactive molecule with substantial anticancer properties and a pharmacological profile optimal for joining the currently available pharmacopeia. In addition, extensive experimental data shows that this chronobiotic agent exerts oncostatic effects throughout all stages of tumor growth, from initial cell transformation to mitigation of malignant progression and metastasis; additionally, melatonin alleviates the side effects and improves the welfare of radio/chemotherapy‐treated patients. Thus, the support of clinicians and oncologists for the use of melatonin in both the treatment and proactive prevention of cancer is gaining strength. Because of its epidemiological importance and symptomatic debut in advanced stages of difficult clinical management, colorectal cancer (CRC) is a preferential target for testing new therapies. In this regard, the development of effective forms of clinical intervention for the improvement of CRC outcome, specifically metastatic CRC, is urgent. At the same time, the need to reduce the costs of conventional anti‐CRC therapy results is also imperative. In light of this status quo, the therapeutic potential of melatonin, and the direct and indirect critical processes of CRC malignancy it modulates, have aroused much interest. To illuminate the imminent future on CRC research, we focused our attention on the molecular mechanisms underlying the multiple oncostatic actions displayed by melatonin in the onset and evolution of CRC and summarized epidemiological evidence, as well as in vitro, in vivo and clinical findings that support the broadly protective potential demonstrated by melatonin.

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Section: Melatonin and P53: The “Cancer Stem Cell Hypothesis”supporting

confidence: 76%

supporting

confidence: 76%

The emergence of melatonin in oncology: Focus on colorectal cancer

Gil‐Martín

Egea

Reíter

et al. 2019

Medicinal Research Reviews

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“…It has previously been demonstrated that melatonin is associated with aging, reproduction, tumor growth and multiple other biological progresses in human cells (12)(13)(14). Our previous study revealed that melatonin can regulate cell apoptosis by inducing ERS in hFOB 1.19 cells (9).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of septin-7 inhibits melatonin-induced cell apoptosis in human fetal osteoblastic cells via suppression of endoplasmic reticulum stress

et al. 2018

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Our previous study demonstrated that melatonin could induce apoptosis in the human fetal osteoblastic (hFOB) 1.19 cell line via induction of endoplasmic reticulum stress (ERS), and recent studies have demonstrated that the expression of septin‑7 (SEPT7) exhibits a positive correlation with the concentration of melatonin. Western blotting demonstrated the expression level of SEPT7 was significantly upregulated in a dose‑dependent manner following treatment with differing concentrations of melatonin compared with the control groups, which did not receive any treatment. The expression of proteins associated with cell apoptosis and endoplasmic reticulum stress (ERS; pro-caspase‑3, cleaved caspase‑3, C/EBP‑homologous protein, 78 kDa glucose‑regulated protein and phosphorylated‑eukaryotic translation initiation factor 2α) were decreased following transfection with SEPT7 overexpression plasmid and increased following transfection with SEPT7 small interfering RNA compared with the control groups. The results of the present study suggest that SEPT7 inhibits melatonin‑induced cell apoptosis via suppression of ERS.

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“…Moreover, melatonin has been shown to inhibit the expression of stemness-related genes, [ 105 , 128 , 129 ] to inhibit stemness-related pathways [ 105 , 106 ] to improve the response to several anticancer therapies [ 102 , 103 , 130 , 131 , 132 , 133 , 134 ], and to inhibit angiogenesis [ 127 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 , 145 , 146 ]. Finally, in Androgen Receptor (AR) and Estrogen Receptor (ER) positive cells, melatonin inhibits the AR [ 54 , 65 , 147 , 148 , 149 ] and ER response [ 128 , 150 , 151 , 152 , 153 ] through different mechanisms either mediated by MT1 or independent of MT1 receptor binding.…”

Section: Oncoprotective Role Of Melatonin: In Vitro Evidencementioning

confidence: 99%

“…Akbarzadeh and co-workers’ recent work showed that ovarian cancer cells responded differently to melatonin treatment (in terms of cell proliferation, morphological changes, and stemness) depending on the composition of the extracellular matrix where they were cultured [ 145 ]. In this work, the authors showed for the first time the role played by mechanical cues in regulating the response of cells to melatonin.…”

Section: A Possible Crosstalk Between Melatonin Signaling and The mentioning

confidence: 99%

Melatonin and Hippo Pathway: Is There Existing Cross-Talk?

Sardo¹,

Muti

Blandino³

et al. 2017

IJMS

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Melatonin is an indolic hormone that regulates a plethora of functions ranging from the regulation of circadian rhythms and antioxidant properties to the induction and maintenance of tumor suppressor pathways. It binds to specific receptors as well as to some cytosolic proteins, leading to several cellular signaling cascades. Recently, the involvement of melatonin in cancer insurgence and progression has clearly been demonstrated. In this review, we will first describe the structure and functions of melatonin and its receptors, and then discuss both molecular and epidemiological evidence on melatonin anticancer effects. Finally, we will shed light on potential cross-talk between melatonin signaling and the Hippo signaling pathway, along with the possible implications for cancer therapy.

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The impact of different extracellular matrices on melatonin effect in proliferation and stemness properties of ovarian cancer cells

Cited by 21 publications

References 37 publications

The emergence of melatonin in oncology: Focus on colorectal cancer

The emergence of melatonin in oncology: Focus on colorectal cancer

Overexpression of septin-7 inhibits melatonin-induced cell apoptosis in human fetal osteoblastic cells via suppression of endoplasmic reticulum stress

Melatonin and Hippo Pathway: Is There Existing Cross-Talk?

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