Follicle-Stimulating Hormone Signaling in Tumor Biology
Summary
Follicle-stimulating hormone (FSH) traditionally mediates gametogenesis via the FSH receptor (FSHR) on ovarian granulosa and testicular Sertoli cells. Recent evidence reveals FSHR expression beyond gonadal tissues, notably on the endothelium of tumour vasculature, tumour‐associated macrophages and within certain carcinoma cells. Engagement of FSH with FSHR activates heterotrimeric G proteins (Gαs and Gαi), leading to modulation of cyclic AMP–protein kinase A, calcium and phosphoinositide 3‐kinase–AKT pathways. These cascades influence cancer hallmarks by promoting angiogenesis, epithelial–mesenchymal transition (EMT), cell survival and metastatic dissemination. In ovarian and breast carcinomas, FSH–FSHR signalling sustains vascular remodelling at the tumour periphery, while in metastatic lesions of lung, breast, colon and prostate origin it marks intratumoural neovessels and macrophage subsets. Mechanistic studies have identified epigenetic regulation of EMT transcription factors via m6A demethylation and stabilisation of mRNAs such as Snail, linking FSH to enhanced invasiveness. The widespread but selective expression of FSHR in malignant contexts affords opportunities for targeted imaging and anti‐FSHR therapies, including antibody‐drug conjugates and peptide‐based inhibitors. Understanding the balance between Gαs‐ and Gαi‐coupled responses may refine therapeutic strategies to disrupt FSH‐driven tumour progression while preserving reproductive function.
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Follicle-Stimulating Hormone Signaling in Tumor Biology publication trend
The graph below shows the total number of articles in follicle-stimulating hormone signaling in tumor biology across all publications each year (not limited to Nature Index journals).
Technical terms
Follicle-Stimulating Hormone (FSH): a glycoprotein gonadotropin secreted by the anterior pituitary that regulates reproductive cell function via FSHR activation.
FSH Receptor (FSHR): a seven‐transmembrane G protein‐coupled receptor that mediates FSH‐induced signalling in gonadal and extragonadal cells.
Epithelial–Mesenchymal Transition (EMT): a phenotypic switch in epithelial cells characterised by loss of polarity and acquisition of migratory, invasive properties.
N6-methyladenosine (m6A) Demethylation: the enzymatic removal of methyl modifications from adenosine bases in mRNA, affecting transcript stability and translation efficiency.
Tumour Vessel Endothelial Cells (TVEC): specialised endothelial cells lining blood vessels within or around tumours, involved in neovascularisation and metastasis.
References
- FSH induces EMT in ovarian cancer via ALKBH5-regulated Snail m6A demethylation. Theranostics (2024).
- Extragonadal FSHR Expression and Function—Is It Real?. Frontiers in Endocrinology (2019).
- FSH regulates fat accumulation and redistribution in aging through the Gαi/Ca2+/CREB pathway. Aging Cell (2015).
- Expression of follicle-stimulating hormone receptor by the vascular endothelium in tumor metastases. BMC Cancer (2013).
- Endothelial follicle-stimulating hormone receptor expression in invasive breast cancer and vascular remodeling at tumor periphery. Journal of Experimental & Clinical Cancer Research (2015).
- Actions and Roles of FSH in Germinative Cells. International Journal of Molecular Sciences (2021).
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