ArticleOncogene2011
P-cadherin cooperates with insulin-like growth factor-1 receptor to promote metastatic signaling of gonadotropin-releasing hormone in ovarian cancer via p120 catenin.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Age at menarche and epithelial ovarian cancer risk: A meta-analysis and Mendelian randomization study.Cancer medicine · 2019Pooled it
- Serum Level of Cadherin-P (CDH3) Is a Novel Predictor of Cardiovascular Events Related to Atherosclerosis in a 3-Year Follow-Up Study.Journal of clinical medicine · 2024Article
- Insulin-like growth factor-1 receptor crosstalk with integrins, cadherins, and the tumor microenvironment: sticking points in understanding IGF1R function in cancer.Endocrine-related cancer · 2023Review
- Cadherin-3 is a novel oncogenic biomarker with prognostic value in glioblastoma.Molecular oncology · 2022Article
- Epithelial-mesenchymal transition: The history, regulatory mechanism, and cancer therapeutic opportunities.MedComm · 2022Review
- Exclusion from spheroid formation identifies loss of essential cell-cell adhesion molecules in colon cancer cells.Scientific reports · 2018Article
- Guidance of Signaling Activations by Cadherins and Integrins in Epithelial Ovarian Cancer Cells.International journal of molecular sciences · 2016Review
- P-cadherin and the journey to cancer metastasis.Molecular cancer · 2015Review
- Article
- Cell adhesion and urothelial bladder cancer: the role of cadherin switching and related phenomena.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- p70 S6 kinase drives ovarian cancer metastasis through multicellular spheroid-peritoneum interaction and P-cadherin/b1 integrin signaling activation.Oncotarget · 2014Article
- Morphological changes of gonadotropin-releasing hormone neurons in the rat preoptic area across puberty.Neural regeneration research · 2014Article
- Beyond E-cadherin: roles of other cadherin superfamily members in cancer.Nature reviews. Cancer · 2014Review
- P-Cadherin Linking Breast Cancer Stem Cells and Invasion: A Promising Marker to Identify an "Intermediate/Metastable" EMT State.Frontiers in oncology · 2014Review
- Targeting gonadotropin-releasing hormone receptor inhibits the early step of ovarian cancer metastasis by modulating tumor-mesothelial adhesion.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Toward an integrative analysis of the tumor microenvironment in ovarian epithelial carcinoma.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012Article
- GPCRs and cancer.Acta pharmacologica Sinica · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gonadotropin-releasing hormone (GnRH) is a potent prometastatic factor in ovarian cancer, but the intracellular signaling events are not well understood. The classical Gα(q)-phospholipase C signal transduction pathway known to operate in the pituitary is not involved in GnRH actions at non-pituitary targets. Here we showed that GnRH treatment of ovarian cancer cells led to a rapid and remarkable tyrosine phosphorylation of p120 catenin (p120(ctn)), which was mediated by P-cadherin. The use of P-cadherin small interfering RNA or neutralizing antibodies to inhibit P-cadherin expression and function resulted in diminished p120(ctn) activation, confirming that the effect was P-cadherin specific. On exploring how P-cadherin, which lacks intrinsic kinase activity, might regulate the activation of p120(ctn), we found that P-cadherin could induce the ligand-independent activation of insulin-like growth factor-1 receptor (IGF-1R). Inhibition of IGF-1R expression or its activity significantly inhibited GnRH-induced p120(ctn) activation, and the subsequent cell migration and invasion. In addition, we showed that IGF-1R regulation by P-cadherin was associated with complex formation between IGF-1R and P-cadherin, and this regulation was also observed to be in vivo correlated with metastasis. Furthermore, using a mouse model of ovarian cancer metastasis, GnRH receptor knockdown was shown to diminish peritoneal dissemination of tumors and ascites formation. These findings suggest for the first time that GnRH can initiate an outside-in p120(ctn) signal transduction through the cross-talk between P-cadherin and IGF-1R, thus providing a novel molecular mechanism by which GnRH may control the high level of aggressiveness and invasion and metastasis potential that are characteristic of ovarian cancer.
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Registered trials
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