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Review
. 2014;18(5):302-6.
doi: 10.5114/wo.2014.43938. Epub 2014 Nov 5.

Is oestrogen an important player in melanoma progression?

Marcelina E Janik  1 , Klaudyna Bełkot  1 , Małgorzata Przybyło  1
Affiliations
Review

Is oestrogen an important player in melanoma progression?

Marcelina E Janik et al. Contemp Oncol (Pozn). 2014.

Abstract

The oestrogen-dependent regulation of cell behaviour is realised by stimulation of specific oestrogen receptors. The classical oestrogen receptors ERα and ERβ are transcription factors, and they modulate expression of hormonally regulated genes, while the third one, GPER, is thought to be responsible for the observed rapid, non-genomic cellular response. Oestrogen dependency is attributed to a number of cancers, including breast, ovarian and endometrial cancer; however, there is still growing evidence that melanoma should also be cited as a hormonally dependent tumour. This comes from the observations of gender-related differences in melanoma progression and reports concerning the history of the malignant course of melanomas during pregnancy. Although, the observations of oestrogen regulation of melanoma progression are controversial, the effect of oestrogen should not be neglected, as the skin possesses its own hormonal microenvironment. This aspect of melanoma progression should be taken under careful consideration as it may offer new therapeutic possibilities.

Keywords: GPER; melanoma; oestrogen; oestrogen receptor α; oestrogen receptor β.

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Figures

Fig. 1
Fig. 1
The mechanism of oestrogen action. The binding of E2 to the classical ERα or ERβ receptors leads to transcription of hormone-dependent genes. The third possible ER, GPER, is a membrane receptor, which is suggested to be responsible for non-genomic E2 action. Activated GPER triggers the clustering of α5β1 integrins, which in turn leads to the assembly of fibronectin matrix. Oestrogen action via GPER is enhanced by the presence of the IGFR-ligand complex, which results in stimulation of the GPER gene transcription. The GPER activation promotes also transactivation of EGFR, resulting in activation of signalling pathway, also leading to GPER gene transcription. Another possible way of E2 action is through hERα-36/-46, which are shorter isoforms of ERα localised in plasma membrane. Their function is not yet fully understood
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