ArticleCancer research2011
Haploinsufficiency in the prometastasis Kiss1 receptor Gpr54 delays breast tumor initiation, progression, and lung metastasis.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- GPR54 regulates non-small cell lung cancer development via dopa decarboxylase.Signal transduction and targeted therapy · 2026Article
- Kisspeptin Receptor Agonists and Antagonists: Strategies for Discovery and Implications for Human Health and Disease.International journal of molecular sciences · 2025Review
- The neuroscience of cancer: Focus on neuropeptidergic systems.Acta pharmaceutica Sinica. B · 2025Review
- YAP/TAZ activation predicts clinical outcomes in mesothelioma and is conserved in in vitro model of driver mutations.Clinical and translational medicine · 2023Article
- 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
- Article
- KISS1 protein expression is associated with worse prognosis in osteosarcoma patients: a long-term follow-up study.Translational cancer research · 2019Article
- Autocrine production of reproductive axis neuropeptides affects proliferation of canine osteosarcoma in vitro.BMC cancer · 2019Article
- The matrix protein Fibulin-3 promotes KISS1R induced triple negative breast cancer cell invasion.Oncotarget · 2018Article
- LGR4 modulates breast cancer initiation, metastasis, and cancer stem cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Controversial Role of Kisspeptins/KiSS-1R Signaling System in Tumor Development.Frontiers in endocrinology · 2018Review
- KISS1/KISS1R in Cancer: Friend or Foe?Frontiers in endocrinology · 2018Review
- Retinoblastoma protein (Rb) links hypoxia to altered mechanical properties in cancer cells as measured by an optical tweezer.Scientific reports · 2017Article
- G protein-coupled KISS1 receptor is overexpressed in triple negative breast cancer and promotes drug resistance.Scientific reports · 2017Article
- For robust big data analyses: a collection of 150 important pro-metastatic genes.Chinese journal of cancer · 2017Review
- Article
- The effects of kisspeptin-10 on migration and proliferation of endothelial cell.Advanced biomedical research · 2015Article
- The effect of Kisspeptin-10 on mesenchymal stem cells migration in vitro and in vivo.Advanced biomedical research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Activation of KISS1 receptor (KISS1R or GPR54) by its ligands (Kisspeptins) regulates a diverse function both in normal physiology and pathophysiology. In cancer, KISS1R has been implicated in tumor angiogenesis and metastasis, but a broader evaluation of KISS1R in tumorigenesis and tumor progression is yet to be conducted. In this study, we used mouse models of Kiss1r gene knockout and mouse mammary tumor virus-polyoma virus middle T antigen (MMTV-PyMT)-induced breast cancer to conduct such an evaluation. Kiss1r heterozygosity in MMTV-PyMT mice was sufficient to attenuate breast cancer initiation, growth, latency, multiplicity, and lung metastasis. To confirm these effects and assess possible contributions of endogenous ligands, we isolated primary tumor cells from PyMT/Kiss1r(+/+) and PyMT/Kiss1r(+/-) mice and compared their phenotypes by in vitro and in vivo assays. Kiss1r loss attenuated in vitro tumorigenic properties as well as tumor growth in vivo in immunocompromised NOD.SCID/NCr mice. Kiss1r activation in these cells, resulting from the addition of its ligand Kisspeptin-10, resulted in RhoA activation and RhoA-dependent gene expression through the Gαq-p63RhoGEF signaling pathway. Anchorage-independent growth was tightly linked to dose-dependent regulation of RhoA by Kiss1r. In support of these results, siRNA-mediated knockdown of KISS1R or inactivation of RhoA in human MCF10A breast epithelial cells overexpressing H-RasV12 was sufficient to reduce Ras-induced anchorage-independent growth. In summary, we concluded that Kiss1r attenuation was sufficient to delay breast tumor initiation, progression, and metastasis through inhibitory effects on the downstream Gαq-p63RhoGEF-RhoA signaling pathway.
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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.