ArticlePloS one2011
GPR54 (KISS1R) transactivates EGFR to promote breast cancer cell invasiveness.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
47 citing papers in PubMed, 95 citations in OpenAlex.
- The neuroscience of cancer: Focus on neuropeptidergic systems.Acta pharmaceutica Sinica. B · 2025Review
- AMH and Kisspeptin Receptor Expression in Rare Hydropic Leiomyoma: A Case Study.The American journal of case reports · 2025Article
- The MET Oncogene Network of Interacting Cell Surface Proteins.International journal of molecular sciences · 2024Review
- The IQGAP scaffolds: Critical nodes bridging receptor activation to cellular signaling.The Journal of cell biology · 2023Review
- Article
- A Novel Splice Variant ofCancers · 2022Article
- Lack of Oestrogen Receptor Expression in Breast Cancer Cells Does Not Correlate with Kisspeptin Signalling and Migration.International journal of molecular sciences · 2022Article
- Targeting hepatic kisspeptin receptor ameliorates nonalcoholic fatty liver disease in a mouse model.The Journal of clinical investigation · 2022Article
- Endocytosis: a pivotal pathway for regulating metastasis.British journal of cancer · 2021Review
- KISS1 in metastatic cancer research and treatment: potential and paradoxes.Cancer metastasis reviews · 2020Review
- Role of the tumor microenvironment in regulating the anti-metastatic effect of KISS1.Clinical & experimental metastasis · 2020Review
- G protein-coupled kisspeptin receptor induces metabolic reprograming and tumorigenesis in estrogen receptor-negative breast cancer.Cell death & disease · 2020Article
- Structure and function of β-arrestins, their emerging role in breast cancer, and potential opportunities for therapeutic manipulation.Advances in cancer research · 2020Article
- KISS1 in breast cancer progression and autophagy.Cancer metastasis reviews · 2019Review
- Complex Formation between VEGFR2 and the βCell chemical biology · 2019Article
- Therapeutic targeting of HER2-CBProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Autocrine production of reproductive axis neuropeptides affects proliferation of canine osteosarcoma in vitro.BMC cancer · 2019Article
- The Endocannabinoid System as a Target in Cancer Diseases: Are We There Yet?Frontiers in pharmacology · 2019Review
- New Routes in GPCR/β-Arrestin-Driven Signaling in Cancer Progression and Metastasis.Frontiers in pharmacology · 2019Review
- BRET-based assay to monitor EGFR transactivation by the ATBiochemical pharmacology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Kisspeptins (Kp), peptide products of the Kisspeptin-1 (KISS1) gene are endogenous ligands for a G protein-coupled receptor 54 (GPR54). Previous findings have shown that KISS1 acts as a metastasis suppressor in numerous cancers in humans. However, recent studies have demonstrated that an increase in KISS1 and GPR54 expression in human breast tumors correlates with higher tumor grade and metastatic potential. At present, whether or not Kp signaling promotes breast cancer cell invasiveness, required for metastasis and the underlying mechanisms, is unknown. We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays. Furthermore, Kp-10 stimulated an increase in matrix metalloprotease (MMP)-9 activity. We also found that Kp-10 induced the transactivation of epidermal growth factor receptor (EGFR). Knockdown of the GPCR scaffolding protein, β-arrestin 2, inhibited Kp-10-induced EGFR transactivation as well as Kp-10 induced invasion of breast cancer cells via modulation of MMP-9 secretion and activity. Finally, we found that the two receptors associate with each other under basal conditions, and FRET analysis revealed that GPR54 interacts directly with EGFR. The stability of the receptor complex formation was increased upon treatment of cells by Kp-10. Taken together, our findings suggest a novel mechanism by which Kp signaling via GPR54 stimulates breast cancer cell invasiveness.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.