{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Moody TW"],"funding":["Intramural NIH HHS","This work is partially supported by the Intramural Research Program of the NIDDK, NIH. DK05-3101-29."],"pagination":["1225"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12467189"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(9)"],"pubmed_abstract":["The bombesin (Bn) receptor family [Gastrin-releasing peptide (GRPR/BB2R) and Neuromedin B receptors (NMBR/BB1R)] are G-protein coupled receptors (GPCR's) with potent growth effects on normal tissues/numerous cancers, often by transactivating the ErbB receptor-tyrosine kinase (RTK) family. Whereas GRPR stimulation transactivates ErbB RTKs EGFR, HER2, and HER3 in non-small cell lung-cancer (NSCLC) cells, its effects on HER4 are unknown. This study was designed to address this question. Of 12 NSCLC's studied, 75% had HER4 mRNA expression and Western-Blotting. NCI-H522 and NCI-H661-cells had high levels of GRPR, HER4, and the HER4-ligand neuregulin (NRG1). Adding GRP to NCI-H522/NCI-H661-cells activated HER4, shown by its increased phosphorylation (P-HER4). The GRPR antagonists PD176252/BW2258"],"journal":["Biology"],"pubmed_title":["Gastrin-Releasing Peptide Receptors Stimulate MAPK-Mediated Growth of Lung Cancer Cells by Transactivating HER4 in a Neuregulin-1, MAP Kinase-Dependent Manner Requiring Activation of the ROS-System."],"pmcid":["PMC12467189"],"funding_grant_id":["Z01 DK053101","DK05-3101-29."],"pubmed_authors":["Moody TW","Jensen RT","Iordanskaia T","Mantey SA","Ramos-Alvarez I"],"additional_accession":[]},"is_claimable":false,"name":"Gastrin-Releasing Peptide Receptors Stimulate MAPK-Mediated Growth of Lung Cancer Cells by Transactivating HER4 in a Neuregulin-1, MAP Kinase-Dependent Manner Requiring Activation of the ROS-System.","description":"The bombesin (Bn) receptor family [Gastrin-releasing peptide (GRPR/BB2R) and Neuromedin B receptors (NMBR/BB1R)] are G-protein coupled receptors (GPCR's) with potent growth effects on normal tissues/numerous cancers, often by transactivating the ErbB receptor-tyrosine kinase (RTK) family. Whereas GRPR stimulation transactivates ErbB RTKs EGFR, HER2, and HER3 in non-small cell lung-cancer (NSCLC) cells, its effects on HER4 are unknown. This study was designed to address this question. Of 12 NSCLC's studied, 75% had HER4 mRNA expression and Western-Blotting. NCI-H522 and NCI-H661-cells had high levels of GRPR, HER4, and the HER4-ligand neuregulin (NRG1). Adding GRP to NCI-H522/NCI-H661-cells activated HER4, shown by its increased phosphorylation (P-HER4). The GRPR antagonists PD176252/BW2258","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-05-02T03:18:06.282Z","creation":"2026-05-02T03:09:56.361Z"},"accession":"S-EPMC12467189","cross_references":{"pubmed":["41007372"],"doi":["10.3390/biology14091225"]}}