Abstract
Osteosarcoma, the most common primary bone malignancy, occurs most frequently in adolescents with a peak of incidence at 11–15 years. Melatonin, an indole amine hormone, shows a wide range of anticancer activities. The decrease in melatonin levels simultaneously concurs with the increase in bone growth and the peak age distribution of osteosarcoma during puberty, so melatonin has been utilized as an adjunct to chemotherapy to improve the quality of life and clinical outcomes. While a large amount of research has been conducted to understand the complex pleiotropic functions and the molecular and cellular actions elicited by melatonin in various types of cancers, a few review reports have focused on osteosarcoma. Herein, we summarized the anti-osteosarcoma effects of melatonin and its underlying molecular mechanisms to illustrate the known significance of melatonin in osteosarcoma and to address cellular signaling pathways of melatonin in vitro and in animal models. Even in the same kind of osteosarcoma, melatonin has been sparingly investigated to counteract tumor growth, apoptosis, and metastasis through different mechanisms, depending on different cell lines. We highlighted the underlying mechanism of anti-osteosarcoma properties evoked by melatonin, including antioxidant activity, anti-proliferation, induction of apoptosis, and the inhibition of invasion and metastasis. Moreover, we discussed the drug synergy effects of the role of melatonin involved and the method to fortify the anti-cancer effects on osteosarcoma. As a potential therapeutic agent, melatonin is safe for children and adolescents and is a promising candidate for an adjuvant by reinforcing the therapeutic effects and abolishing the unwanted consequences of chemotherapies.
Highlights
Cancer is a well-known public health problem associated with high mortality and disability rates worldwide [1]
MG-63 cells and other malignant and non-malignant bone tumors has been demonstrated [62], and these and MG-63 cells and other malignant and non-malignant bone tumors has been demonstrated [62], and findings suggest an irreplaceable role for MT1 in bone pathology (Figure 3). In human osteosarcoma these findings suggest an irreplaceable role for MT1 in bone pathology (Figure 3)
U2OS and HOS cell-derived C motif chemokine ligand 24 (CCL24) contributes to cellular invasion and migration through the upstream Jun N-terminal kinase (JNK) signaling pathway; this finding implies a promotional role of CCL24 in osteosarcoma metastasis; the action is inhibited by melatonin
Summary
Cancer is a well-known public health problem associated with high mortality and disability rates worldwide [1]. Osteosarcoma is the most prevalent primary bone cancer with a peak of incidence at 10–15 years and the second incidence peak in older adulthood [3,4,5]. This malignant bone tumor often first develops in. Cells 2019, 8, 1618 the second incidence peak in older adulthood [3,4,5] This malignant bone tumor often first develops in the metaphysis of long and proximal about six in everychildren million the metaphysis of long bonesbones (distal(distal femurfemur and proximal tibia) intibia) aboutinsix in every million children twomillion in every million [6].
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