ArticleOncogene2015
Cross talk between the bombesin neuropeptide receptor and Sonic hedgehog pathways in small cell lung carcinoma.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- The underexplored links between cancer and the internal body climate: Implications for cancer prevention and treatment.Frontiers in oncology · 2022Pooled it
- The neuroscience of cancer: Focus on neuropeptidergic systems.Acta pharmaceutica Sinica. B · 2025Review
- GPCR-Gα13 Involvement in Mitochondrial Function, Oxidative Stress, and Prostate Cancer.International journal of molecular sciences · 2024Review
- Bombesin-drug conjugates in targeted therapy for small cell lung cancer.American journal of cancer research · 2022Review
- GαFrontiers in cell and developmental biology · 2022Review
- Coagulation Signaling through PAR1 as a Therapeutic Target in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2021Review
- Gα-13 induces CThe Journal of biological chemistry · 2019Article
- Carcinogenesis and Reactive Oxygen Species Signaling: Interaction of the NADPH Oxidase NOX1-5 and Superoxide Dismutase 1-3 Signal Transduction Pathways.Antioxidants & redox signaling · 2019Review
- Isolation and characterization of adrenocortical progenitors involved in the adaptation to stress.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- PM2.5 promotes human bronchial smooth muscle cell migration via the sonic hedgehog signaling pathway.Respiratory research · 2018Article
- Article
- Expression of progenitor markers is associated with the functionality of a bioartificial adrenal cortex.PloS one · 2018Article
- Review
- Exploiting cancer's phenotypic guise against itself: targeting ectopically expressed peptide G-protein coupled receptors for lung cancer therapy.Oncotarget · 2017Review
- How gastrin-releasing peptide receptor (GRPR) and αScientific reports · 2017Article
- A novel therapeutic approach against B-cell non-Hodgkin's lymphoma through co-inhibition of Hedgehog signaling pathway and autophagy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Metformin increases antitumor activity of MEK inhibitors through GLI1 downregulation in LKB1 positive human NSCLC cancer cells.Oncotarget · 2016Article
- The Hedgehog Signaling Networks in Lung Cancer: The Mechanisms and Roles in Tumor Progression and Implications for Cancer Therapy.BioMed research international · 2016Review
- Shh and p50/Bcl3 signaling crosstalk drives pathogenesis of BCCs in Gorlin syndrome.Oncotarget · 2015Article
- Sonic Hedgehog in SCLC.Aging · 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 4 institutions in 2 countries.
Funding
Abstract
Small cell lung carcinoma (SCLC) often features the upregulation of the Sonic hedgehog (Shh) pathway leading to activation of Gli transcription factors. SCLC cells secrete bombesin (BBS)-like neuropeptides that act as autocrine growth factors. Here, we show that SCLC tumor samples feature co-expression of Shh and BBS-cognate receptor (gastrin-releasing peptide receptor (GRPR)). We also demonstrate that BBS activates Gli in SCLC cells, which is crucial for BBS-mediated SCLC proliferation, because cyclopamine, an inhibitor of the Shh pathway, hampered the BBS-mediated effects. BBS binding to GRPR stimulated Gli through its downstream Gαq and Gα₁₂/₁₃ GTPases, and consistently, other Gαq and Gα₁₃ coupled receptors (such as muscarinic receptor, m1, and thrombin receptor, PAR-1) and constitutively active GαqQL and Gα₁₂/₁₃QL mutants stimulated Gli. By using cells null for Gαq and Gα₁₂/₁₃, we demonstrate that these G proteins are strictly necessary for Gli activation by BBS. Moreover, by using constitutively active Rho small G-protein (Rho QL) as well as its inhibitor, C3 toxin, we show that Rho mediates G-protein-coupled receptor (GPCR)-, Gαq- and Gα₁₂/₁₃-dependent Gli stimulation. At the molecular level, BBS caused a significant increase in Shh gene transcription and protein secretion that was dependent on BBS-induced GPCR/Gαq-₁₂/₁₃/Rho mediated activation of nuclear factor κB (NFκB), which can stimulate a NF-κB response element in the Shh gene promoter. Our data identify a novel molecular network acting in SCLC linking autocrine BBS and Shh circuitries and suggest Shh inhibitors as novel therapeutic strategies against this aggressive cancer type.
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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.