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Abstract
Simple SummaryThe ongoing clinical need to improve cancer therapies warrants a better understanding of the mechanisms behind cancer growth and its spread to distant organs. To this end, research into the impact of sex hormones, such as oestrogens and testosterones, in cancers has led to improvements in the way sex hormone-responsive cancers are treated. Pigment epithelium-derived factor (PEDF) is a protein with anti-cancer properties that is also sensitive to sex hormones. The aim of this review is to explore what is currently known about sex hormones and PEDF in cancers in order to better understand the anti-cancer role of PEDF in sex hormone-responsive cancers.Oestrogens and androgens play important roles in normal and cancerous tissue and have been shown to negatively regulate pigment epithelium-derived factor (PEDF) expression in sex hormone-responsive tumours. PEDF suppresses tumour growth and its downregulation by oestrogen is implicated in tumorigenesis, metastasis, and progression. PEDF expression is reduced in cancerous tissue of the prostate, breast, ovary, and endometrium compared to their normal tissue counterparts, with a link between PEDF downregulation and sex hormone signalling observed in pre-clinical studies. PEDF reduces growth and metastasis of tumour cells by promoting apoptosis, inhibiting angiogenesis, increasing adhesion, and reducing migration. PEDF may also prevent treatment resistance in some cancers by downregulating oestrogen receptor signalling. By interacting with components of the tumour microenvironment, PEDF counteracts the proliferative and immunosuppressive effects of oestrogens, to ultimately reduce tumorigenesis and metastasis. In this review, we focus on sex hormone regulation of PEDF’s anti-tumour action in sex hormone-responsive tumours.
Highlights
Sex hormones including oestrogens, progesterone, and androgens play important roles in regulating development and physiological function [1,2,3]
Motif receptor 1; ER: oestrogen receptor; ERK: extracellular signal regulated kinase; FAK: focal adhesion kinase; FasL: Fas ligand; HIF: hypoxia inducible factor; Il: interleukin; JNK: c-Jun N-terminal kinase; LR; laminin receptor; matrix metalloproteinases (MMPs): matrix metalloproteinase; mTOR: mammalian target of rapamycin; NF-κB: nuclear factor-kappa B; PI3K: phosphoinositide 3-kinases; plasminogen inhibitor activator (PAI)-2: plasminogen activator inhibitor-2; PPAR-γ: peroxisome proliferator-activated receptor-gamma; Pigment epithelium-derived factor (PEDF)-R: PEDF receptor; RET: receptor tyrosine kinase rearranged during transfection; uPA: urokinase plasminogen activator; uPAR: uPA receptor; VEGF: vascular endothelial growth factor; ↑↑: increases;
It is expected that the potential prognostic role of PEDF across a diverse range of cancers may be better defined with larger studies focused on specific tumour types, with larger patient numbers and patient outcome data being available
Summary
Progesterone, and androgens play important roles in regulating development and physiological function [1,2,3]. Aberrant sex hormone signalling is implicated in tumorigenesis, metastasis, progression, and treatment resistance in cancers arising in sex hormone-responsive tissues [4].
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