Nowadays, cancer has become one of the major killers threatening human health, and the role of sex hormones in the occurrence and development of cancer has attracted widespread attention. In recent years, with the rise of precision medicine, scientists have gradually realized that there are significant differences in treatment response and disease progression among cancer patients of different genders and ages. This discovery has triggered scientists to explore in depth how sex hormones affect cancer behavior.
Recently, in a research report entitled "Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin" published in the international journal Nature, scientists from Paris Sciences et Alpes Research University and other institutions revealed the relationship between sex hormone receptors and cancer metastasis through research, especially the key role of GRPR (gastrin-releasing peptide receptor). The relevant research results may provide new ideas for cancer treatment.
In this study, the researchers aimed to reveal how sex hormones regulate the metastatic ability of cancer by affecting the expression of specific receptors. By deeply analyzing the role of E-cadherin in sex hormone signaling, they discovered a new pathway connecting sex hormones and cancer metastasis. This discovery not only deepens our understanding of the mechanism of cancer metastasis, but also provides a theoretical basis and experimental foundation for the development of new anti-cancer therapies.
The researchers used mouse melanoma models as the main experimental subjects, and combined them with human melanoma and breast cancer samples for analysis. The experiment used a variety of technical means such as gene editing technology (such as CRISPR-Cas9), cell culture, animal model construction, RNA sequencing, ChIP-seq, etc., and conducted in-depth research on the expression and function of key molecules such as E-cadherin, GRPR, and ERα (estrogen receptor α).
Figure 1. GRPR activates YAP1 to activate the metastatic program. (Raymond, Jérémy H., et al. 2025)
First, they constructed a mouse melanoma model with conditional knockout of E-cadherin and observed the effect of E-cadherin deficiency on tumor metastasis. Then, RNA sequencing and ChIP-seq techniques revealed changes in gene expression profiles in tumor cells after E-cadherin deficiency, especially the up-regulated expression of GRPR and ERα. To further verify these findings, the researchers also conducted relevant analyses in human melanoma and breast cancer samples and explored the effects of sex hormones on GRPR expression in these samples.
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The results showed that the loss of E-cadherin leads to the activation of the B-catenin signaling pathway, which in turn upregulates the expression of ERα and GRPR. GRPR activation promotes tumor cell invasion and metastasis through the Gaq/11-PKC-YAP1 signaling axis. In addition, sex hormones (especially estrogen) can further affect the expression and activity of GRPR by regulating ERα. These findings indicate that there is a close connection between the sex hormone signaling pathway and cancer metastasis, and GRPR may become a new target for anticancer therapy.
In this study, researchers revealed for the first time the important role of sex hormone receptors (such as GRPR) in cancer metastasis and elucidated the molecular mechanism behind it. This discovery not only challenges our traditional understanding of cancer metastasis, but also provides new ideas for the development of anti-cancer therapies targeting sex hormone receptors. In the future, researchers will further explore the potential of GRPR inhibitors in cancer treatment to bring more effective and safe treatment options to patients.
Reference
- Raymond, Jérémy H., et al. Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin. Nature (2025): 1-9.