ArticleMolecular cancer research : MCR2012
The essential role of Giα2 in prostate cancer cell migration.
Article in Molecular cancer research : MCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Suppression of GNAI2 message in ovarian cancer.Journal of ovarian research · 2014Pooled it
- Exploring the Toxicological Impact and Mechanisms of DEHP Exposure on Prostate Cancer Through Network Toxicology and Machine Learning Algorithms.Current medicinal chemistry · 2026Article
- Preclinical Development of GT-14, a Novel Inhibitor of GαThe AAPS journal · 2025Article
- GαInternational journal of molecular sciences · 2025Article
- Target repositioning using multi-layer networks and machine learning: The case of prostate cancer.Computational and structural biotechnology journal · 2024Article
- Development and validation of a sensitive LC-MS/MS assay of GT-14, a novel GαJournal of pharmaceutical and biomedical analysis · 2024Article
- GαCancers · 2024Article
- G-protein signaling of oxytocin receptor as a potential target for cabazitaxel-resistant prostate cancer.PNAS nexus · 2024Article
- Follicle-Stimulating Hormone Induces Lipid DropletsFrontiers in endocrinology · 2021Article
- Small Molecule Inhibitors Targeting GαCancers · 2020Article
- Differential roles and activation of mammalian target of rapamycin complexes 1 and 2 during cell migration in prostate cancer cells.The Prostate · 2020Article
- Novel role of Giα2 in cell migration: Downstream of PI3-kinase-AKT and Rac1 in prostate cancer cells.Journal of cellular physiology · 2018Article
- The function of oxytocin: a potential biomarker for prostate cancer diagnosis and promoter of prostate cancer.Oncotarget · 2017Article
- MicroRNA-222-3p/GNAI2/AKT axis inhibits epithelial ovarian cancer cell growth and associates with good overall survival.Oncotarget · 2016Article
- Bioinformatics analyses of significant prognostic risk markers for thyroid papillary carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cell- and receptor-specific regulation of cell migration by Gi/oα-proteins remains unknown in prostate cancer cells. In the present study, oxytocin (OXT) receptor was detected at the protein level in total cell lysates from C81 (an androgen-independent subline of LNCaP), DU145 and PC3 prostate cancer cells, but not in immortalized normal prostate luminal epithelial cells (RWPE1), and OXT-induced migration of PC3 cells. This effect of OXT has been shown to be mediated by Gi/oα-dependent signaling. Accordingly, OXT inhibited forskolin-induced luciferase activity in PC3 cells that were transfected with a luciferase reporter for cyclic AMP activity. Although mRNAs for all three Giα isoforms were present in PC3 cells, Giα2 was the most abundant isoform that was detected at the protein level. Pertussis toxin (PTx) inhibited the OXT-induced migration of PC3 cells. Ectopic expression of the PTx-resistant Giα2-C352G, but not wild-type Giα2, abolished this effect of PTx on OXT-induced cell migration. The Giα2-targeting siRNA was shown to specifically reduce Giα2 mRNA and protein in prostate cancer cells. The Giα2-targeting siRNA eliminated OXT-induced migration of PC3 cells. These data suggest that Giα2 plays an important role in the effects of OXT on PC3 cell migration. The Giα2-targeting siRNA also inhibited EGF-induced migration of PC3 and DU145 cells. Expression of the siRNA-resistant Giα2, but not wild type Giα2, restored the effects of EGF in PC3 cells transfected with the Giα2-targeting siRNA. In conclusion, Giα2 plays an essential role in OXT and EGF signaling to induce prostate cancer cell migration.
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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.