Melatonin suppresses epithelial‑to‑mesenchymal transition in the MG‑63 cell line

Chen, Yongjun; Zhang, Tao; Liu, Xiongwei; Li, Zengyan; Zhou, Dongming; Xu, Wenqing

doi:10.3892/mmr.2019.10902

Cited by 9 publications

(8 citation statements)

References 38 publications

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“…Similar results were also obtained in osteosarcoma MG-63 cells, where results pointed toward a role of melatonin in suppressing the EMT via HIF-1α/Snail/MMP-9 signaling. These studies revealed that the melatonin treatment caused an increase in the ratio of E-cadherin/N-cadherin in tumor cells while suppressing Snail and MMP-9 levels [ 123 ]. Additionally, in vitro studies using human HCT15 and SW620 colorectal cancer cells showed that the melatonin treatment had a regulatory effect on E-cadherin and Snail-expression levels while exerting weak cytotoxicity [ 124 ].…”

Section: Melatonin As An Inhibitor Of the Epithelial-to-mesenchymal T...mentioning

confidence: 99%

Melatonin and Its Role in the Epithelial-to-Mesenchymal Transition (EMT) in Cancer

Martínez-Campa,

Álvarez-García,

Alonso-González

et al. 2024

Cancers

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The epithelial-to-mesenchymal transition (EMT) is a cell-biological program that occurs during the progression of several physiological processes and that can also take place during pathological situations such as carcinogenesis. The EMT program consists of the sequential activation of a number of intracellular signaling pathways aimed at driving epithelial cells toward the acquisition of a series of intermediate phenotypic states arrayed along the epithelial–mesenchymal axis. These phenotypic features include changes in the motility, conformation, polarity and functionality of cancer cells, ultimately leading cells to stemness, increased invasiveness, chemo- and radioresistance and the formation of cancer metastasis. Amongst the different existing types of the EMT, type 3 is directly involved in carcinogenesis. A type 3 EMT occurs in neoplastic cells that have previously acquired genetic and epigenetic alterations, specifically affecting genes involved in promoting clonal outgrowth and invasion. Markers such as E-cadherin; N-cadherin; vimentin; and transcription factors (TFs) like Twist, Snail and ZEB are considered key molecules in the transition. The EMT process is also regulated by microRNA expression. Many miRNAs have been reported to repress EMT-TFs. Thus, Snail 1 is repressed by miR-29, miR-30a and miR-34a; miR-200b downregulates Slug; and ZEB1 and ZEB2 are repressed by miR-200 and miR-205, respectively. Occasionally, some microRNA target genes act downstream of the EMT master TFs; thus, Twist1 upregulates the levels of miR-10b. Melatonin is an endogenously produced hormone released mainly by the pineal gland. It is widely accepted that melatonin exerts oncostatic actions in a large variety of tumors, inhibiting the initiation, progression and invasion phases of tumorigenesis. The molecular mechanisms underlying these inhibitory actions are complex and involve a great number of processes. In this review, we will focus our attention on the ability of melatonin to regulate some key EMT-related markers, transcription factors and micro-RNAs, summarizing the multiple ways by which this hormone can regulate the EMT. Since melatonin has no known toxic side effects and is also known to help overcome drug resistance, it is a good candidate to be considered as an adjuvant drug to conventional cancer therapies.

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Section: Melatonin As An Inhibitor Of the Epithelial-to-mesenchymal T...mentioning

confidence: 99%

Melatonin and Its Role in the Epithelial-to-Mesenchymal Transition (EMT) in Cancer

Martínez-Campa,

Álvarez-García,

Alonso-González

et al. 2024

Cancers

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“…Curcumin suppresses colon cancer growth and metastasis, associated with upregulated epithelial markers and downregulated mesenchymal markers as well as EMT-related transcription factors Snail and Twist [ 102 ]. Chen et al showed that the anticancer effects of melatonin on osteosarcoma OA MG-63 cells were mediated by the inhibition of EMT through the HIF-1α/Snail/MMP 9 signaling pathways [ 103 ]. Prostate cancer stem cells with a mesenchymal phenotype are triggered by cancer-associated fibroblasts (CAFs) by HIF-1α/β-catenin-dependent signaling pathways [ 104 ].…”

Section: Ps Involvement In Tumor Metastasis By Mediating Coagulationmentioning

confidence: 99%

Microparticle Phosphatidylserine Mediates Coagulation: Involvement in Tumor Progression and Metastasis

Jing

Xiang

et al. 2023

Cancers

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Tumor progression and cancer metastasis has been linked to the release of microparticles (MPs), which are shed upon cell activation or apoptosis and display parental cell antigens, phospholipids such as phosphatidylserine (PS), and nucleic acids on their external surfaces. In this review, we highlight the biogenesis of MPs as well as the pathophysiological processes of PS externalization and its involvement in coagulation activation. We review the available evidence, suggesting that coagulation factors (mainly tissue factor, thrombin, and fibrin) assist in multiple steps of tumor dissemination, including epithelial–mesenchymal transition, extracellular matrix remodeling, immune escape, and tumor angiogenesis to support the formation of the pre-metastatic niche. Platelets are not just bystander cells in circulation but are functional players in primary tumor growth and metastasis. Tumor-induced platelet aggregation protects circulating tumor cells (CTCs) from the blood flow shear forces and immune cell attack while also promoting the binding of CTCs to endothelial cells and extravasation, which activates tumor invasion and sustains metastasis. Finally, in terms of therapy, lactadherin can inhibit coagulation by competing effectively with coagulation factors for PS binding sites and may similarly delay tumor progression. Furthermore, we also investigate the therapeutic potential of coagulation factor inhibitors within the context of cancer treatment. The development of multiple therapies targeting platelet activation and platelet–tumor cell interactions may not only reduce the lethal consequences of thrombosis but also impede tumor growth and spread.

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“…In addition, melatonin was found to suppress RSK2 via the HER2/MAPK/Erk pathway to inhibit EMT in breast cancer cells [ 148 ]. Besides these pathways, melatonin has also been shown to inhibit transforming growth factor beta-induced EMT in MG-63 osteosarcoma cells via the HIF-1/Snail/MMP-9 pathway [ 149 ].…”

Section: Potential Therapeutic Mechanisms Of Melatonin In Endometriosismentioning

confidence: 99%

Melatonin in Endometriosis: Mechanistic Understanding and Clinical Insight

Hung

Zhang

et al. 2022

Nutrients

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Endometriosis is defined as the development of endometrial glands and stroma outside the uterine cavity. Pathophysiology of this disease includes abnormal hormone profiles, cell survival, migration, invasion, angiogenesis, oxidative stress, immunology, and inflammation. Melatonin is a neuroendocrine hormone that is synthesized and released primarily at night from the mammalian pineal gland. Increasing evidence has revealed that melatonin can be synthesized and secreted from multiple extra-pineal tissues where it regulates immune response, inflammation, and angiogenesis locally. Melatonin receptors are expressed in the uterus, and the therapeutic effects of melatonin on endometriosis and other reproductive disorders have been reported. In this review, key information related to the metabolism of melatonin and its biological effects is summarized. Furthermore, the latest in vitro and in vivo findings are highlighted to evaluate the pleiotropic functions of melatonin, as well as to summarize its physiological and pathological effects and treatment potential in endometriosis. Moreover, the pharmacological and therapeutic benefits derived from the administration of exogenous melatonin on reproductive system-related disease are discussed to support the potential of melatonin supplements toward the development of endometriosis. More clinical trials are needed to confirm its therapeutic effects and safety.

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Melatonin suppresses epithelial‑to‑mesenchymal transition in the MG‑63 cell line

Cited by 9 publications

References 38 publications

Melatonin and Its Role in the Epithelial-to-Mesenchymal Transition (EMT) in Cancer

Melatonin and Its Role in the Epithelial-to-Mesenchymal Transition (EMT) in Cancer

Microparticle Phosphatidylserine Mediates Coagulation: Involvement in Tumor Progression and Metastasis

Melatonin in Endometriosis: Mechanistic Understanding and Clinical Insight

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