---
title: "GPR52 loss promotes multicellular reorganization and collective invasion in breast cancer"
id: "british-journal-of-cancer-1-role-of-orphan-g-protein-coupled-receptor-gpr52-in-breast-cancer-cell"
canonical_url: "https://medichelpline.com/clinical-feed/british-journal-of-cancer-1-role-of-orphan-g-protein-coupled-receptor-gpr52-in-breast-cancer-cell"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03565-0"
published_at: "2026-08-20T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# GPR52 loss promotes multicellular reorganization and collective invasion in breast cancer
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/british-journal-of-cancer-1-role-of-orphan-g-protein-coupled-receptor-gpr52-in-breast-cancer-cell
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03565-0)
- **Published At:** 2026-08-20T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The orphan **GPCR GPR52** is downregulated in many solid tumours and further reduced in breast cancer metastases compared with primary tumours. Low tumour GPR52 mRNA associates with worse overall survival, especially in **triple-negative breast cancer (TNBC)**. - CRISPR–Cas9 knockout (KO) of GPR52 was generated in TNBC lines MDA-MB-468 and MDA-MB-231, and in non-tumorigenic MCF10A cells to study functional effects. - GPR52 loss increased intracellular **cAMP** levels and elevated phosphorylation of **CREB**, consistent with upregulated cAMP signalling identified by RNA-sequencing and proteomics of GPR52-null cells. - In 2D culture, GPR52 KO cells formed tighter cell–cell interactions and clusters; transmission electron microscopy showed altered cell–cell interface length and cellular proximity at contacts. - On extracellular matrix substrates, GPR52 KO cells adopted more spindle-like, mesenchymal morphologies (poly-D-lysine, collagen) and altered 3D spheroid architecture in Matrigel. - GPR52-null breast cancer cells had an increased propensity for collective organisation and collective invasion in 3D Matrigel cultures. - Zebrafish xenografts injected with GPR52 KO cells developed greater total cancer area than control-injected fish, indicating increased tumour burden in vivo. - Re-expression of GPR52 or pharmacologic inhibition of cAMP production rescued several GPR52 KO phenotypes, supporting a mechanistic role for cAMP signalling downstream of GPR52 loss. - The data suggest that loss of GPR52 may be a mechanism promoting multicellular reorganisation, hybrid/partial EMT features, and progression in breast cancer, and support exploration of **GPR52 agonism** as a therapeutic strategy.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [british journal of cancer](https://www.nature.com/bjc) 3. [articles](https://www.nature.com/bjc/articles?type=article) 4. article Role of orphan G protein-coupled receptor GPR52 in breast cancer cell multicellular organization and collective invasion [ Download PDF ](https://www.nature.com/articles/s41416-026-03565-0.pdf) [ Download PDF ](https://www.nature.com/articles/s41416-026-03565-0.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 20 August 2026 Translational Therapeutics # Role of orphan G protein-coupled receptor GPR52 in breast cancer cell multicellular organization and collective invasion * [Sarah Z. Hanif](https://www.nature.com/articles/s41416-026-03565-0#auth-Sarah_Z_-Hanif-Aff1-Aff2)[1](https://www.nature.com/articles/s41416-026-03565-0#Aff1),[2](https://www.nature.com/articles/s41416-026-03565-0#Aff2), * [Caleb Kutz](https://www.nature.com/articles/s41416-026-03565-0#auth-Caleb-Kutz-Aff3-Aff4)[3](https://www.nature.com/articles/s41416-026-03565-0#Aff3),[4](https://www.nature.com/articles/s41416-026-03565-0#Aff4), * [CheukMan Cherie Au](https://www.nature.com/articles/s41416-026-03565-0#auth-CheukMan_Cherie-Au-Aff2)[2](https://www.nature.com/articles/s41416-026-03565-0#Aff2), * [Ingrid Torregroza](https://www.nature.com/articles/s41416-026-03565-0#auth-Ingrid-Torregroza-Aff5)[5](https://www.nature.com/articles/s41416-026-03565-0#Aff5), * [Sailesh Palikhe](https://www.nature.com/articles/s41416-026-03565-0#auth-Sailesh-Palikhe-Aff3-Aff4)[3](https://www.nature.com/articles/s41416-026-03565-0#Aff3),[4](https://www.nature.com/articles/s41416-026-03565-0#Aff4), * [Syeda Y. Jannath](https://www.nature.com/articles/s41416-026-03565-0#auth-Syeda_Y_-Jannath-Aff2-Aff6)[2](https://www.nature.com/articles/s41416-026-03565-0#Aff2),[6](https://www.nature.com/articles/s41416-026-03565-0#Aff6), * [Tabassum Fabiha](https://www.nature.com/articles/s41416-026-03565-0#auth-Tabassum-Fabiha-Aff7)[7](https://www.nature.com/articles/s41416-026-03565-0#Aff7), * [Bhavneet Bhinder](https://www.nature.com/articles/s41416-026-03565-0#auth-Bhavneet-Bhinder-Aff8)[8](https://www.nature.com/articles/s41416-026-03565-0#Aff8), * [Michael P. Washburn](https://www.nature.com/articles/s41416-026-03565-0#auth-Michael_P_-Washburn-Aff3-Aff9)[3](https://www.nature.com/articles/s41416-026-03565-0#Aff3),[9](https://www.nature.com/articles/s41416-026-03565-0#Aff9), * [Dominic Devost](https://www.nature.com/articles/s41416-026-03565-0#auth-Dominic-Devost-Aff10)[10](https://www.nature.com/articles/s41416-026-03565-0#Aff10), * [Shuchen Liu](https://www.nature.com/articles/s41416-026-03565-0#auth-Shuchen-Liu-Aff2)[2](https://www.nature.com/articles/s41416-026-03565-0#Aff2), * [Priya Bhardwaj](https://www.nature.com/articles/s41416-026-03565-0#auth-Priya-Bhardwaj-Aff2)[2](https://www.nature.com/articles/s41416-026-03565-0#Aff2), * [Todd Evans](https://www.nature.com/articles/s41416-026-03565-0#auth-Todd-Evans-Aff5)[5](https://www.nature.com/articles/s41416-026-03565-0#Aff5), * [Xiaobo Liang](https://www.nature.com/articles/s41416-026-03565-0#auth-Xiaobo-Liang-Aff4)[4](https://www.nature.com/articles/s41416-026-03565-0#Aff4), * [Pradeep Kumar Anand](https://www.nature.com/articles/s41416-026-03565-0#auth-Pradeep_Kumar-Anand-Aff11)[11](https://www.nature.com/articles/s41416-026-03565-0#Aff11), * [Robert Tarran](https://www.nature.com/articles/s41416-026-03565-0#auth-Robert-Tarran-Aff11)[11](https://www.nature.com/articles/s41416-026-03565-0#Aff11), * [Olivier Elemento](https://www.nature.com/articles/s41416-026-03565-0#auth-Olivier-Elemento-Aff8) [ORCID: orcid.org/0000-0002-8061-9617](https://orcid.org/0000-0002-8061-9617)[8](https://www.nature.com/articles/s41416-026-03565-0#Aff8), * [Lukas E. Dow](https://www.nature.com/articles/s41416-026-03565-0#auth-Lukas_E_-Dow-Aff2-Aff12-Aff13) [ORCID: orcid.org/0000-0001-7048-1418](https://orcid.org/0000-0001-7048-1418)[2](https://www.nature.com/articles/s41416-026-03565-0#Aff2),[12](https://www.nature.com/articles/s41416-026-03565-0#Aff12),[13](https://www.nature.com/articles/s41416-026-03565-0#Aff13), * [John Blenis](https://www.nature.com/articles/s41416-026-03565-0#auth-John-Blenis-Aff12-Aff13-Aff14)[12](https://www.nature.com/articles/s41416-026-03565-0#Aff12),[13](https://www.nature.com/articles/s41416-026-03565-0#Aff13),[14](https://www.nature.com/articles/s41416-026-03565-0#Aff14), * [Terence E. Hébert](https://www.nature.com/articles/s41416-026-03565-0#auth-Terence_E_-H_bert-Aff10)[10](https://www.nature.com/articles/s41416-026-03565-0#Aff10) & * … * [Kristy A. Brown](https://www.nature.com/articles/s41416-026-03565-0#auth-Kristy_A_-Brown-Aff2-Aff3-Aff4) [ORCID: orcid.org/0000-0003-3382-5546](https://orcid.org/0000-0003-3382-5546)[2](https://www.nature.com/articles/s41416-026-03565-0#Aff2),[3](https://www.nature.com/articles/s41416-026-03565-0#Aff3),[4](https://www.nature.com/articles/s41416-026-03565-0#Aff4) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03565-0#citeas) [ Save article ](https://www.nature.com/articles/s41416-026-03565-0/save-research?_csrf=a03C27L3i64KDEntWsEB6fX7N-UowWQm) [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background G protein-coupled receptors (GPCRs) are the largest class of membrane-bound receptors and are emerging as targets for the effective treatment of cancer. The role of orphan GPCR GPR52 in cancer has not been characterized. Low mRNA expression of GPR52 in breast tumours correlates with reduced overall survival, leading to the hypothesis that loss of GPR52 supports breast cancer progression. ### Methods CRISPR-Cas9 was used to knock out GPR52 in the human triple-negative breast cancer cell lines MDA-MB-468 and MDA-MB-231. 2D and 3D in vitro studies, electron microscopy, and a zebrafish xenograft model were used to assess the morphology and behaviour of GPR52 KO cells. ### Results Loss of GPR52 was associated with elevated levels of cAMP, increased cell–cell interaction in 2D cultures, more spindle-like morphology on collagen, altered 3D spheroid morphology, and increased propensity to organize and invade collectively. Zebrafish injected with GPR52 KO cells developed a greater total cancer area than control. RNA sequencing and proteomic analyses of GPR52-null cells revealed an increased cAMP signalling signature. Re-expression of GPR52 and inhibition of cAMP production rescued some GPR52 KO phenotypes. ### Conclusions GPR52 loss is a potential mechanism by which breast cancer progression may occur and supports the investigation of GPR52 agonism as a therapeutic option for breast cancer. ### Statement of Significance Loss of the orphan GPCR GPR52 in human breast cell lines leads to increased cell clustering, hybrid/partial EMT, and increased tumour burden in zebrafish, further expanding our understanding of mechanisms driving cancer progression and opening the door to novel therapeutic approaches. ## Background Metastasis is the primary cause of death in breast cancer patients [[1](https://www.nature.com/articles/s41416-026-03565-0#ref-CR1 "Hagemeister FB Jr, Buzdar AU, Luna MA, Blumenschein GR. Causes of death in breast cancer: a clinicopathologic study. Cancer. 1980;46:162–7.")]. The process required for cancer cells of solid tumours to metastasize is intensive, and cells undergo several adaptive processes to enhance their metastatic potential. These include changes in cell–cell and cell-matrix adhesion, transitions between epithelial and mesenchymal cell states, and the ability to degrade and invade tissues [[2](https://www.nature.com/articles/s41416-026-03565-0#ref-CR2 "Schuster E, Taftaf R, Reduzzi C, Albert MK, Romero-Calvo I, Liu H. Better together: circulating tumor cell clustering in metastatic cancer. Trends Cancer. 2021;7:1020–32."), [3](https://www.nature.com/articles/s41416-026-03565-0#ref-CR3 "Bakir B, Chiarella AM, Pitarresi JR, Rustgi AK. EMT, MET, plasticity, and tumor metastasis. Trends Cell Biol. 2020;30:764–76.")]. However, the upstream regulators of these processes are not well characterized, which limits mechanistic understanding and therapeutic intervention. G protein-coupled receptors (GPCRs) are the largest protein family encoded by the human genome [[4](https://www.nature.com/articles/s41416-026-03565-0#ref-CR4 "Venter JC, Adams MD, Myers EW, Li PW, Mural RJ, Sutton GG, et al. The sequence of the human genome. Science. 2001;291:1304–51.")]. These receptors consist of an extracellular N-terminus followed by seven transmembrane α-helices, which are connected by three intracellular and three extracellular loops and a cytoplasmic C-terminal tail [[5](https://www.nature.com/articles/s41416-026-03565-0#ref-CR5 "Hanson MA, Stevens RC. Discovery of new GPCR biology: one receptor structure at a time. Structure. 2009;17:8–14.")]. Their transmembrane structure enables the transmission of critical signals between extracellular and intracellular spaces. Dissociation of the heterotrimeric G protein upon GPCR activation can regulate a diverse array of downstream molecules, allowing for the regulation of various cell processes, including proliferation, migration, adhesion, and metabolism [[6](https://www.nature.com/articles/s41416-026-03565-0#ref-CR6 "Hamm HE, Gilchrist A. Heterotrimeric G proteins. Curr Opin Cell Biol. 1996;8:189–96."), [7](https://www.nature.com/articles/s41416-026-03565-0#ref-CR7 "Chaudhary PK, Kim S. An Insight into GPCR and G-Proteins as Cancer Drivers. Cells. 2021;10:3288.")]. GPR52 is a structurally unique GPCR that is enriched in the basal ganglia, and its endogenous ligand remains unknown, rendering it an orphan receptor [[8](https://www.nature.com/articles/s41416-026-03565-0#ref-CR8 "Komatsu H, Maruyama M, Yao S, Shinohara T, Sakuma K, Imaichi S, et al. Anatomical transcriptome of G protein-coupled receptors leads to the identification of a novel therapeutic candidate GPR52 for psychiatric disorders. PLoS One. 2014;9:e90134.")]. It has garnered increased attention in recent years owing to its potential as a neurotherapeutic target for schizophrenia and Huntington’s disease [[9](https://www.nature.com/articles/s41416-026-03565-0#ref-CR9 "Nishiyama K, Suzuki H, Harasawa T, Suzuki N, Kurimoto E, Kawai T, et al. FTBMT, a novel and selective GPR52 agonist, demonstrates antipsychotic-like and procognitive effects in rodents, revealing a potential therapeutic agent for schizophrenia. J Pharmacol Exp Ther. 2017;363:253–64."), [10](https://www.nature.com/articles/s41416-026-03565-0#ref-CR10 "Yao Y, Cui X, Al-Ramahi I, Sun X, Li B, Hou J, et al. A striatal-enriched intronic GPCR modulates huntingtin levels and toxicity. Elife. 2015;4:e05449.")]. We examined GPR52 mRNA levels in 19 solid tumour types and determined that GPR52 is significantly downregulated in tumour samples [[11](https://www.nature.com/articles/s41416-026-03565-0#ref-CR11 "Bartha A, Gyorffy B. TNMplot.com: a web tool for the comparison of gene expression in normal, tumor and metastatic tissues. Int J Mol Sci. 2021;22:2622.")]. However, the role of GPR52 in cancer progression has not been reported. In patients with breast cancer, we found that GPR52 expression was further reduced in metastases compared with that in the primary tumour [[11](https://www.nature.com/articles/s41416-026-03565-0#ref-CR11 "Bartha A, Gyorffy B. TNMplot.com: a web tool for the comparison of gene expression in normal, tumor and metastatic tissues. Int J Mol Sci. 2021;22:2622.")]. Low GPR52 mRNA expression in resected triple-negative breast cancer (TNBC) is also associated with a reduction in overall survival [[12](https://www.nature.com/articles/s41416-026-03565-0#ref-CR12 "Gyorffy B. Survival analysis across the entire transcriptome identifies biomarkers with the highest prognostic power in breast cancer. Comput Struct Biotechnol J. 2021;19:4101–9.")]. We generated GPR52 KO breast epithelial cells from the widely used TNBC MDA-MB-468 and MDA-MB-231, and the non-cancerous MCF10A lines. Loss of GPR52 led to an increase in cell–cell interactions in 2D cultures, with the formation of cell clusters in each cell line. Transmission electron microscopy (TEM) of WT and GPR52 KO cells revealed differences in cell–cell adhesion properties, including the length of the cell–cell interface and the proximity of cells along this interface. In 3D Matrigel cultures, GPR52 KO was associated with changes in the organization and morphology of MDA-MB-468 and MDA-MB-231 spheroids. Furthermore, GPR52 loss increased the propensity of breast cancer cells to organize and invade collectively when cultured in Matrigel. Lastly, we found that the culture of GPR52 KO cells on poly-D-lysine or collagen led to a more mesenchymal phenotype. Loss of GPR52 was associated with an increase in intracellular cAMP levels, and RNA-sequencing and proteomic studies of GPR52-null cells demonstrated the upregulation of several pathways implicated in breast cancer, including cAMP signalling [[13](https://www.nature.com/articles/s41416-026-03565-0#ref-CR13 "Au CC, Furness JB, Britt K, Oshchepkova S, Ladumor H, Soo KY, et al. Three-dimensional growth of breast cancer cells potentiates the anti-tumor effects of unacylated ghrelin and AZP-531. Elife. 2020;9:e56913.")]. Furthermore, we found that phosphorylation of CREB was increased in GPR52 KO cells and that re-expression of GPR52 or inhibition of cAMP production rescued some of the GPR52 KO phenotypes. Overall, our results revealed that GPR52 loss is a potential mechanism by which important processes in breast cancer progression, such as changes in multicellular organization, may occur. These processes have long been implicated in many solid tumours; however, critical and targetable upstream regulators have not been identified. As GPCRs are the targets of more than 1/3 of FDA-approved small-molecule drugs, these data support the investigation of GPR52 agonism as a viable therapeutic approach in breast cancer [[14](https://www.nature.com/articles/s41416-026-03565-0#ref-CR14 "Sriram K, Insel PA. G protein-coupled receptors as targets for approved drugs: How many targets and how many drugs?. Mol Pharmacol. 2018;93:251–8.")]. ## Results ### GPR52 expression is reduced in cancerous tissue compared to normal, and inversely associated with breast cancer prognosis and metastatic potential To date, there have been no reports on the role of GPR52 in any type of cancer. However, GPR52 mRNA expression levels have been reported in many transcriptome profiles of resected cancerous and noncancerous tissues. We compared GPR52 mRNA expression levels in normal and tumour samples from the tissues from which solid tumours arose (Fig. [1a](https://www.nature.com/articles/s41416-026-03565-0#Fig1)) using the TNMplot webtool [[11](https://www.nature.com/articles/s41416-026-03565-0#ref-CR11 "Bartha A, Gyorffy B. TNMplot.com: a web tool for the comparison of gene expression in normal, tumor and metastatic tissues. Int J Mol Sci. 2021;22:2622.")]. We found that, in the majority of these tissue types, GPR52 mRNA expression levels were lower in tumours than in non-cancerous samples (Fig. [1a](https://www.nature.com/articles/s41416-026-03565-0#Fig1), _P_ < 0.05, indicated with an asterisk). Importantly, low tumour GPR52 mRNA expression was found to be associated with a reduction in overall survival in patients with breast cancer (Fig. [1b](https://www.nature.com/articles/s41416-026-03565-0#Fig1)), with the impact of low GPR52 on survival being more pronounced for triple-negative breast cancer (TNBC) (Fig. [1c](https://www.nature.com/articles/s41416-026-03565-0#Fig1)) [[12](https://www.nature.com/articles/s41416-026-03565-0#ref-CR12 "Gyorffy B. Survival analysis across the entire transcriptome identifies biomarkers with the highest prognostic power in breast cancer. Comput Struct Biotechnol J.
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