Oncotarget

Research Papers:

Oleoylethanolamide inhibits α-melanocyte stimulating hormone-stimulated melanogenesis via ERK, Akt and CREB signaling pathways in B16 melanoma cells

Juan Zhou, Tong Ren, Ying Li, Anran Cheng, Wanyi Xie, Lanxi Xu, Lu Peng, Jinbin Lin, Lianxiang Lian, Yong Diao, Xin Jin _ and Lichao Yang

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Oncotarget. 2017; 8:56868-56879. https://doi.org/10.18632/oncotarget.18097

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Abstract

Juan Zhou1,*, Tong Ren1,*, Ying Li2,*, Anran Cheng3, Wanyi Xie3, Lanxi Xu3, Lu Peng3, Jinbin Lin3, Lianxiang Lian3, Yong Diao4, Xin Jin3 and Lichao Yang3

1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, Xiamen University, Xiamen, China

2Department of Pharmacy, Xiamen Medical College, Xiamen, China

3Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, Xiamen, China

4School of Biomedical Sciences, Huaqiao University, Quanzhou, China

*These authors have contributed equally to this work and should be considered co-first authors

Correspondence to:

Xin Jin, email: [email protected]

Lichao Yang, email: [email protected]

Keywords: oleoylethanolamide, melanin, tyrosinase, α-melanocyte stimulating hormone, B16 mouse melanoma cell

Received: January 17, 2017     Accepted: April 11, 2017     Published: May 23, 2017

ABSTRACT

The present study aimed to examine the potential inhibitory activity of oleoylethanolamide (OEA) on α-melanocyte stimulating hormone (α-MSH)-stimulated melanogenesis and the molecular mechanism(s) involved in the process in B16 mouse melanoma cells. Our data demonstrated that OEA markedly inhibited melanin synthesis and tyrosinase activity in α-MSH-stimulated B16 cells. In addition, the expression of melanogenesis-related proteins, such as melanocortin-1 receptor (MC1R), microphthalmia-associated transcription factor (MITF), tyrosinase-related protein-1 (TRP-1) and tyrosinase, was suppressed in a concentration-dependent manner by OEA. In addition, OEA may suppress melanogenesis through a peroxisome proliferator-activated receptor α (PPARα)-independent pathway. Moreover, OEA activated ERK, Akt, p38 pathways and inhibits CREB pathway in α-MSH-stimulated B16 cells. The specific ERK inhibitor PD98059 partly blocked OEA-inhibited melanin synthesis and tyrosinase activity and partly abrogated the OEA-suppressed expression of melanogenic proteins. Furthermore, OEA presented remarkable inhibition on the body pigmentation in the zebrafish model system. Our findings demonstrated that OEA is an effective inhibitor of hyperpigmentation through activation of ERK, Akt and p38 pathways, inhibition of the CREB pathway, and subsequent down-regulation of MITF, TRP-1 and tyrosinase production.


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