{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Huisman DH"],"funding":["National Cancer Institute (NCI)","U.S. Department of Defense","U.S. Department of Defense (DOD)","National Cancer Institute","NCI NIH HHS","Nebraska Department of Health and Human Services (Nebraska DHHS)","Nebraska Department of Health and Human Services","National Institute of General Medical Sciences","NIGMS NIH HHS","National Institute of General Medical Sciences (NIGMS)"],"pagination":["640-652"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12221803"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(7)"],"pubmed_abstract":["Small cell lung carcinoma (SCLC) tumors are heterogeneous, with a subpopulation of cells primed for tumor initiation. In this study, we show that kinase suppressor of Ras 2 (KSR2) promotes the self-renewal and clonogenicity of SCLC cells. KSR2 is a molecular scaffold that promotes Raf/MEK/ERK signaling. KSR2 is preferentially expressed in the ASCL1 subtype of SCLC (SCLC-A) tumors and is expressed in pulmonary neuroendocrine cells, one of the identified cells of origin for SCLC-A tumors. The expression of KSR2 in SCLC and pulmonary neuroendocrine cells was previously unrecognized and serves as a novel model for understanding the role of KSR2-dependent signaling in normal and malignant tissues. Disruption of KSR2 in SCLC-A cell lines inhibits the colony-forming ability of tumor-propagating c"],"journal":["Molecular cancer research : MCR"],"pubmed_title":["KSR2 Promotes Self-Renewal and Clonogenicity of Small Cell Lung Carcinoma."],"pmcid":["PMC12221803"],"funding_grant_id":["P30 CA036727","F30 CA268766","U24 CA213274","NIH GM121316 and CA277495","P20 GM121316","LC210123","LB 506","R01 CA277495","P50 CA070907","P20 GM103427","P30CA036727","R21CA256638","R21 CA256638","U24CA213274"],"pubmed_authors":["Huisman DH","Skupa S","Chatterjee D","Minna JD","Svoboda RA","Ireland AS","Lewis RE","Vieira HM","Frodyma DE","Oliver TG","Askew JW","Girard L","Kareta MS","Fisher KW"],"additional_accession":[]},"is_claimable":false,"name":"KSR2 Promotes Self-Renewal and Clonogenicity of Small Cell Lung Carcinoma.","description":"Small cell lung carcinoma (SCLC) tumors are heterogeneous, with a subpopulation of cells primed for tumor initiation. In this study, we show that kinase suppressor of Ras 2 (KSR2) promotes the self-renewal and clonogenicity of SCLC cells. KSR2 is a molecular scaffold that promotes Raf/MEK/ERK signaling. KSR2 is preferentially expressed in the ASCL1 subtype of SCLC (SCLC-A) tumors and is expressed in pulmonary neuroendocrine cells, one of the identified cells of origin for SCLC-A tumors. The expression of KSR2 in SCLC and pulmonary neuroendocrine cells was previously unrecognized and serves as a novel model for understanding the role of KSR2-dependent signaling in normal and malignant tissues. Disruption of KSR2 in SCLC-A cell lines inhibits the colony-forming ability of tumor-propagating c","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-06-06T09:00:36.981Z","creation":"2026-05-28T03:10:49.635Z"},"accession":"S-EPMC12221803","cross_references":{"pubmed":["40063515"],"doi":["10.1158/1541-7786.mcr-24-0546","10.1158/1541-7786.MCR-24-0546"]}}