ArticleFrontiers in pharmacology2022
The olfactory receptor OR51E2 activates ERK1/2 through the Golgi-localized Gβγ-PI3Kγ-ARF1 pathway in prostate cancer cells.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Ectopic Olfactory Receptors in Oral Health and Disease: Molecular Links Between Chemosensing, Tissue Repair, Inflammation, and Cancer.International journal of molecular sciences · 2026Review
- An interpretable deep learning biomarker for prognostication and prediction of adjuvant chemotherapy benefit in gastric cancer.NPJ precision oncology · 2026Article
- THRESHOLD: a comprehensive transcriptomic analysis tool for evaluating gene saturation and impact in disease progression.NAR cancer · 2025Article
- Overcoming research bias: The untapped potential of biomedically important but understudied proteins.iScience · 2025Article
- The olfactory receptor OR51E2 regulates prostate cancer aggressiveness and modulates STAT3 in prostate cancer cells and in xenograft tumors.BMC cancer · 2025Article
- A review of research advances in the modulation of olfactory receptors for COPD inflammation and airway remodeling.Frontiers in immunology · 2025Review
- G protein-coupled receptors in prostate cancer: research progress and therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- Article
- Deciphering olfactory receptor binding mechanisms: a structural and dynamic perspective on olfactory receptors.Frontiers in molecular biosciences · 2024Review
- Article
- Non-canonical Golgi-compartmentalized Gβγ signaling: mechanisms, functions, and therapeutic targets.Trends in pharmacological sciences · 2023Review
- Identification of a novel senescence-associated signature to predict biochemical recurrence and immune microenvironment for prostate cancer.Frontiers in immunology · 2023Article
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Authors and funding
3 authors.
Funding
Abstract
The olfactory receptor OR51E2 is ectopically expressed in prostate tissues and regulates prostate cancer progression, but its function and regulation in oncogenic mitogen-activate protein kinase (MAPK) activation are poorly defined. Here we demonstrate that β-ionone, an OR51E2 agonist, dose-dependently activates extracellular signal-regulated kinases 1 and 2 (ERK1/2) in prostate cancer cells, with an EC50 value of approximate 20 μM and an efficiency comparable to other receptor agonists. We also find that CRISPR-Cas9-mediated knockout of Golgi-translocating Gγ9 subunit, phosphoinositide 3-kinase γ (PI3Kγ) and the small GTPase ADP-ribosylation factor 1 (ARF1), as well as pharmacological inhibition of Gβγ, PI3Kγ and Golgi-localized ARF1, each abolishes ERK1/2 activation by β-ionone. We further show that β-ionone significantly promotes ARF1 translocation to the Golgi and activates ARF1 that can be inhibited by Gγ9 and PI3Kγ depletion. Collectively, our data demonstrate that OR51E2 activates ERK1/2 through the Gβγ-PI3Kγ-ARF1 pathway that occurs spatially at the Golgi, and also provide important insights into MAPK hyper-activation in prostate cancer.
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