Publication date: Jun 24, 2025
They compared melanoma development and progression in mice with and without functional E-cadherin, across sexes. Results showed no difference in initial melanoma onset or primary tumor growth. Editors have highlighted the following attributes while ensuring the content’s credibility:a) In primary melanoma, the loss of CDH1 activates -catenin signaling, subsequently triggering the upregulation of ESR1. c) ECADneg/GRPRpos melanoma cells gain the ability to disseminate through the bloodstream to distant organs, notably the lungs, where GRP is produced in abundance. b) ECADneg/GRPRpos cancer cells grow in tissues expressing naturally GRP including lung, breast and gastric tissue. You’ll get an ad-free account as a thank-you. More information: Jrmy H. Raymond et al, Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin, Nature (2025). Activated GRPR increased cell growth, resistance to cell death (anoikis), and invasivenessall key processes required for metastasis. In normal cells, E-cadherin restricts the transcriptional activity of -catenin. When E-cadherin is lost, -catenin activates the ER gene (ESR1), whose protein indirectly enhances GRPR expression.
| Concepts | Keywords |
|---|---|
| Authors | Cadherin |
| Cancer | Cancers |
| Pharmacological | Catenin |
| Grpr | |
| Hormone | |
| Loss | |
| Melanoma | |
| Metastasis | |
| Nature | |
| Pathway | |
| Receptor | |
| Sex | |
| Specific | |
| Women |
Semantics
| Type | Source | Name |
|---|---|---|
| disease | MESH | breast cancer |
| pathway | KEGG | Breast cancer |
| drug | DRUGBANK | Fulvestrant |
| disease | MESH | cancer |
| disease | MESH | melanoma |
| pathway | KEGG | Melanoma |
| disease | MESH | metastasis |