Melatonin Suppresses Oral Squamous Cell Carcinomas Migration and Invasion through Blocking FGF19/FGFR 4 Signaling Pathway

Wang, Leilei; Su, Yu‐xiong; Choi, Wonyoung

doi:10.3390/ijms22189907

Cited by 9 publications

(2 citation statements)

References 47 publications

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“…Lastly, melatonin abolishes the invasion and migration abilities of SCC-15 cells while decreasing Fibroblast Growth Factor 19 (FGF19) in oral squamous carcinoma cells (SCC-15). The addition of exogenous hFGF19 appears to revoke the effect of the indolamine on cell invasion and migration, whereas FGF19 knockdown mimics the effect of the melatonin treatment [ 170 ].…”

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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“…In the tumor progression phase, the growth and invasion of tumor cells increase rapidly. Melatonin could inhibit cancer cell growth and downregulate matrix metallopeptidase 9 (MMP-9) [ 34 ] and fibroblast growth factor 19 (FGF19) [ 35 ] to inhibit cancer cells’ invasion and migration. Moreover, in vivo studies have demonstrated that melatonin alleviates cancer progression by inactivating Notch homolog 1 (Notch 1) receptor [ 36 ], suppressing estrogen/ubiquitin C/SDHB-mediated succinate accumulation [ 37 ], inhibiting MMP-13 [ 38 ], and downregulating receptor activator of nuclear factor kappa-Β ligand (RANKL) expression levels [ 39 ].…”

Section: Anticancer Effect Of Melatoninmentioning

confidence: 99%

Use of Melatonin in Cancer Treatment: Where Are We?

Wang

Choi

2022

IJMS

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Cancer represents a large group of diseases accounting for nearly 10 million deaths each year. Various treatment strategies, including surgical resection combined with chemotherapy, radiotherapy, and immunotherapy, have been applied for cancer treatment. However, the outcomes remain largely unsatisfying. Melatonin, as an endogenous hormone, is associated with the circadian rhythm moderation. Many physiological functions of melatonin besides sleep–wake cycle control have been identified, such as antioxidant, immunomodulation, and anti-inflammation. In recent years, an increasing number of studies have described the anticancer effects of melatonin. This has drawn our attention to the potential usage of melatonin for cancer treatment in the clinical setting, although huge obstacles still exist before its wide clinical administration is accepted. The exact mechanisms behind its anticancer effects remain unclear, and the specific characters impede its in vivo investigation. In this review, we will summarize the latest advances in melatonin studies, including its chemical properties, the possible mechanisms for its anticancer effects, and the ongoing clinical trails. Importantly, challenges for the clinical application of melatonin will be discussed, accompanied with our perspectives on its future development. Finally, obstacles and perspectives of using melatonin for cancer treatment will be proposed. The present article will provide a comprehensive foundation for applying melatonin as a preventive and therapeutic agent for cancer treatment.

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Pineal Gland Hormone Melatonin Inhibits Migration of Hematopoietic Stem/Progenitor Cells (HSPCs) by Downregulating Nlrp3 Inflammasome and Upregulating Heme Oxygenase-1 (HO-1) Activity

Abdelbaset-Ismail,

Brzezniakiewicz-Janus,

Thapa

et al. 2023

Stem Cell Rev and Rep

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Melatonin Suppresses Oral Squamous Cell Carcinomas Migration and Invasion through Blocking FGF19/FGFR 4 Signaling Pathway

Cited by 9 publications

References 47 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

Use of Melatonin in Cancer Treatment: Where Are We?

Pineal Gland Hormone Melatonin Inhibits Migration of Hematopoietic Stem/Progenitor Cells (HSPCs) by Downregulating Nlrp3 Inflammasome and Upregulating Heme Oxygenase-1 (HO-1) Activity

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