Melatonin and Mesenchymal Stem Cells as a Key for Functional Integrity for Liver Cancer Treatment

Elmahallawy, Ehab Kotb; Mohamed, Yasser; Abdo, Walied; Yanai, Tokuma

doi:10.3390/ijms21124521

Cited by 17 publications

(9 citation statements)

References 168 publications

(228 reference statements)

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“…Therefore, it is highly suggestive that the restoration of cardiac glucose utilization revealed in this study was a result of a melatonin‐induced attenuation of ventricular hypertrophy that was observed in a prior study 19 . Consistent with our findings, several previous studies also found that melatonin suppressed glycolysis in various types of cancer cells, leading to a delay in tumor growth and increased chemosensitivity 42–46 . For this reason, it is possible that melatonin itself can protect against doxorubicin‐induced heart failure by limiting the utilization of cardiac glucose.…”

Section: Discussionsupporting

confidence: 91%

“…19 Consistent with our findings, several previous studies also found that melatonin suppressed glycolysis in various types of cancer cells, leading to a delay in tumor growth and increased chemosensitivity. [42][43][44][45][46] For this reason, it is possible that melatonin itself can protect against doxorubicin-induced heart failure by limiting the utilization of cardiac glucose. To support this statement, a future study using a rat model pretreated with melatonin is needed.…”

Section: Doxorubicin Increased Mitochondrial Oxidative Stress In Embr...mentioning

confidence: 99%

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Effects of melatonin on cardiac metabolic reprogramming in doxorubicin‐induced heart failure rats: A metabolomics study for potential therapeutic targets

Thonusin

Nawara

Arinno

et al. 2023

Journal of Pineal Research

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Using mass spectrometry-based targeted metabolomics, we aimed to determine the pattern of cardiac metabolic reprogramming and energetics in doxorubicin-induced heart failure. More importantly, we aimed to identify the potential effects of melatonin on cardiac metabolic reprogramming and energetics in doxorubicin-induced heart failure. Male Wistar rats (n = 18) were randomly divided into three groups (n = 6/group) to receive either (1) normal saline solution as a control, (2) 3 mg/kg/day of doxorubicin on Days 0, 4, 8, 15, 22, and 29, or (3) 3 mg/kg/day of doxorubicin on Days 0, 4, 8, 15, 22, and 29 plus 10 mg/kg/day of melatonin on Days 0-29. On Day 30, echocardiography was carried out and heart rate variability was analyzed for the evaluation of cardiac function. The rats were euthanized on the following day to enable the collection of ventricular cardiac tissue. Compared to the control group, the hearts of rats treated with doxorubicin alone exhibited impaired cardiac function, increased glucose and ketone body utilization, decreased fat utilization, decreased succinate oxidation, and decreased production of adenosine triphosphate. The cotreatment with melatonin could restore cardiac function, glucose and ketone body utilization, and adenosine triphosphate production in the heart. Interestingly, the cotreatment with melatonin led to an increase in cardiac fatty acid oxidation, branched-chain amino acid catabolism, and anaplerosis. All of these findings highlighted the potential efficacy of melatonin with regard to cardiac metabolic reprogramming and energetics. Our findings also suggested that melatonin could be considered as an adjunctive treatment for doxorubicin-induced heart failure in clinical practice.

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Section: Discussionsupporting

confidence: 91%

Section: Doxorubicin Increased Mitochondrial Oxidative Stress In Embr...mentioning

confidence: 99%

Effects of melatonin on cardiac metabolic reprogramming in doxorubicin‐induced heart failure rats: A metabolomics study for potential therapeutic targets

Thonusin

Nawara

Arinno

et al. 2023

Journal of Pineal Research

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“…Limits of interpretation result from approaches in which CSCs are subjected to combined treatments with melatonin and a cytostatic agent. Another type of combination was applied in hepatocellular carcinoma, in which MSCs were tested for their therapeutic potential in the presence of melatonin [234]. In this case, an increase of apoptosis was reported, something that would be in accordance with experience from applications of melatonin alone in tumor cells.…”

Section: Some Aspects Concerning Cancer Stem Cellssupporting

confidence: 73%

Melatonin and the Programming of Stem Cells

Hardeland

2022

IJMS

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Melatonin interacts with various types of stem cells, in multiple ways that comprise stimulation of proliferation, maintenance of stemness and self-renewal, protection of survival, and programming toward functionally different cell lineages. These various properties are frequently intertwined but may not be always jointly present. Melatonin typically stimulates proliferation and transition to the mature cell type. For all sufficiently studied stem or progenitor cells, melatonin’s signaling pathways leading to expression of respective morphogenetic factors are discussed. The focus of this article will be laid on the aspect of programming, particularly in pluripotent cells. This is especially but not exclusively the case in neural stem cells (NSCs) and mesenchymal stem cells (MSCs). Concerning developmental bifurcations, decisions are not exclusively made by melatonin alone. In MSCs, melatonin promotes adipogenesis in a Wnt (Wingless-Integration-1)-independent mode, but chondrogenesis and osteogenesis Wnt-dependently. Melatonin upregulates Wnt, but not in the adipogenic lineage. This decision seems to depend on microenvironment and epigenetic memory. The decision for chondrogenesis instead of osteogenesis, both being Wnt-dependent, seems to involve fibroblast growth factor receptor 3. Stem cell-specific differences in melatonin and Wnt receptors, and contributions of transcription factors and noncoding RNAs are outlined, as well as possibilities and the medical importance of re-programming for transdifferentiation.

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“…167 Several studies reported that MLT plays significant role in various functions such as endocrine, neural, immune and antioxidant functions both receptor dependent and independent manner. 168 MLT inhibits HepG2 and Hep3B proliferation and cell cycle progression via affecting the cell cycle-associated proteins. MLT potentiates cisplatin-induced apoptosis associated with upregulated caspase-3 and poly ADP-ribose polymerase (PARP) cleavage, as well as Bcl-2 expression.…”

Section: Role and Therapeutic Potential Of Mlt In Liver Cancermentioning

confidence: 99%

Role and Therapeutic Potential of Melatonin in Various Type of Cancers

Gurunathan

Qasim

Kang

et al. 2021

OTT

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Cancer is a large group of diseases and the second leading cause of death worldwide. Lung, prostate, colorectal, stomach, and liver cancers are the most common types of cancer in men, whereas breast, colorectal, lung, cervical, and thyroid cancers are the most common among women. Presently, various treatment strategies, including surgical resection combined with chemotherapy, radiotherapy, nanotherapy, and immunotherapy, have been used as conventional treatments for patients with cancer. However, the clinical outcomes of advanced-stage disease remain relatively unfavorable owing to the emergence of chemoresistance, toxicity, and other undesired detrimental side effects. Therefore, new therapies to overcome these limitations are indispensable. Recently, there has been considerable evidence from experimental and clinical studies suggesting that melatonin can be used to prevent and treat cancer. Studies have confirmed that melatonin mitigates the pathogenesis of cancer by directly affecting carcinogenesis and indirectly disrupting the circadian cycle. Melatonin (MLT) is nontoxic and exhibits a range of beneficial effects against cancer via apoptotic, antiangiogenic, antiproliferative, and metastasis-inhibitory pathways. The combination of melatonin with conventional drugs improves the drug sensitivity of cancers, including solid and liquid tumors. In this manuscript, we will comprehensively review some of the cellular, animal, and human studies from the literature that provide evidence that melatonin has oncostatic and anticancer properties. Further, this comprehensive review compiles the available experimental and clinical data analyzing the history, epidemiology, risk factors, therapeutic effect, clinical significance, of melatonin alone or in combination with chemotherapeutic agents or radiotherapy, as well as the underlying molecular mechanisms of its anticancer effect against lung, breast, prostate, colorectal, skin, liver, cervical, and ovarian cancers. Nonetheless, in the interest of readership clarity and ease of reading, we have discussed the overall mechanism of the anticancer activity of melatonin against different types of cancer. We have ended this report with general conclusions and future perspectives.

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Melatonin and Mesenchymal Stem Cells as a Key for Functional Integrity for Liver Cancer Treatment

Cited by 17 publications

References 168 publications

Effects of melatonin on cardiac metabolic reprogramming in doxorubicin‐induced heart failure rats: A metabolomics study for potential therapeutic targets

Effects of melatonin on cardiac metabolic reprogramming in doxorubicin‐induced heart failure rats: A metabolomics study for potential therapeutic targets

Melatonin and the Programming of Stem Cells

Role and Therapeutic Potential of Melatonin in Various Type of Cancers

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