ArticleLife sciences2014
SR48692 inhibits non-small cell lung cancer proliferation in an EGF receptor-dependent manner.
Article in Life sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
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- Neuropeptide G Protein-Coupled Receptors as Oncotargets.Frontiers in endocrinology · 2018Review
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- The significance of NTR1 expression and its correlation with β-catenin and EGFR in gastric cancer.Diagnostic pathology · 2015Article
- CI-988 Inhibits EGFR Transactivation and Proliferation Caused by Addition of CCK/Gastrin to Lung Cancer Cells.Journal of molecular neuroscience : MN · 2015Article
- Neurotensin receptors in pancreatic ductal carcinomas.EJNMMI research · 2015Article
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- Suppression of the NTS-CPS1 regulatory axis by AFF1 in lung adenocarcinoma cells.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
aimsThe mechanism by which SR48692 inhibits non-small cell lung cancer (NSCLC) proliferation was investigated. MAIN
methodsThe ability of SR48692 to inhibit the proliferation of NSCLC cell lines NCI-H1299 and A549 was investigated in vitro in the presence or absence of neurotensin (NTS). The ability of NTS to cause epidermal growth factor receptor (EGFR) transactivation was investigated by Western blot using NSCLC cells and various inhibitors. The growth effects and Western blot results were determined in cell lines treated with siRNA for NTSR1. KEY
findingsTreatment of A549 or NCI-H1299 cells with siRNA for NTSR1 reduced significantly NTSR1 protein and the ability of SR48692 to inhibit the proliferation of A549 or NCI-H1299 NSCLC cells. Treatment of A549 and NCI-H1299 cells with siRNA for NTSR1 reduced the ability of NTS to cause epidermal growth factor receptor (EGFR) transactivation. SR48692 or gefitinib (EGFR tyrosine kinase inhibitor) inhibited the ability of NTS to cause EGFR and ERK tyrosine phosphorylation. NTS transactivation of the EGFR was inhibited by GM6001 (matrix metalloprotease inhibitor), Tiron (superoxide scavenger) or U73122 (phospholipase C inhibitor) but not H89 (PKA inhibitor). NTS stimulates whereas SR48692 or gefitinib inhibits the clonal growth of NSCLC cells. SIGNIFICANCE: These results suggest that SR48692 may inhibit NSCLC proliferation in an EGFR-dependent mechanism.
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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.