Abstract

Melanogenesis is the sequential process of melanin production by melanocytes in order to protect the skin from harmful stimuli. Melanogenesis is disrupted by radiation exposure, which results in the differentiation of melanocytes into melanoma. Recently, some methods have been developed to maintain the instability of melanogenesis in melanoma by activating cellular autophagy. However, there is still a lack of knowledge about how autophagy is involved in the regulation of melanogenesis in melanoma cells. Here, we used rottlerin as an autophagy inducer to investigate the role of the cyclic adenosine monophosphate (cAMP)/cAMP response element binding (CREB) signaling pathway in melanogenesis. We found that rottlerin can inhibit melanin production by targeting cAMP, which is initially activated by alpha-melanocyte stimulating hormone (α-MSH). Our findings suggest that rottlerin has a pivotal role as an autophagy inducer in the regulation of melanogenesis by targeting the cAMP/CREB signaling pathway.

Highlights

  • Skin is the largest organ of the body and is divided into three layers—comprised of different cell types—the epidermis, dermis, and hypodermis

  • We aimed to investigate the role of rottlerin as an autophagy inducer in the regulation

  • We aimed to investigate the role of rottlerin as an autophagy inducer in the of melanogenesis in melanoma cells

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Summary

Introduction

Skin is the largest organ of the body and is divided into three layers—comprised of different cell types—the epidermis, dermis, and hypodermis. One type of cell in the epidermis produces and stores a dark pigment (melanin) and is called a melanocyte [1]. The function of melanin production is to protect the skin from harmful stimuli such as UV rays, visible light, and infrared irradiation, by absorbing it and transferring it to keratinocytes, which are surrounded by melanocytes, resulting in cell pigmentation and eventually, protection against skin cancers [3,4]. Abnormalities in melanin production and distribution can result in hyperpigmentation by overregulating some dedicated cellular pathways involved in melanogenesis, and transformation of melanocytes into malignant melanoma cells [5]. Many methods to control the regulation of melanogenesis have been studied

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