{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Wang X"],"funding":["NCI NIH HHS"],"pubmed_abstract":["Cytosolic arginine sensor for mTORC1 Subunit 1 (CASTOR1) functions as a key regulator of mechanistic target of rapamycin complex 1 (mTORC1) signaling. Despite its frequent dysregulation in cancers via mechanisms such as KSHV microRNA-mediated inhibition or AKT-driven phosphorylation and degradation, the impact of <i>CASTOR1</i> loss on tumor initiation and progression remains poorly understood. Here, we identify <i>CASTOR1</i> as a critical tumor suppressor in non-small cell lung cancer (NSCLC) by demonstrating that its genetic ablation amplifies tumorigenesis in a <i>KRAS</i>-driven genetically engineered mouse model (GEMM;LSL-<i>KRAS</i> <sup>G12D</sup>). <i>CASTOR1</i> deficiency markedly enhances lung tumor incidence, accelerates tumor progression, and increases proliferative indices i"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2025.04.23.650349"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12045348"],"repository":["biostudies-literature"],"pubmed_title":["&lt;i&gt;CASTOR1&lt;/i&gt;: A Novel Tumor Suppressor Linking mTORC1 and KRAS Pathways in Tumorigenesis and Resistance to KRAS-Targeted Therapies in Non-Small Cell Lung Cancer."],"pmcid":["PMC12045348"],"funding_grant_id":["P30 CA047904","R01 CA124332","R01 CA291244","R01 CA284554","R01 CA096512","R01 CA278812"],"pubmed_authors":["Loo SK","Gao SJ","Huang Y","Li T","Wang MT","Sun S","Chen L","Pennathur A","Wang X","Ding L"],"additional_accession":[]},"is_claimable":false,"name":"&lt;i&gt;CASTOR1&lt;/i&gt;: A Novel Tumor Suppressor Linking mTORC1 and KRAS Pathways in Tumorigenesis and Resistance to KRAS-Targeted Therapies in Non-Small Cell Lung Cancer.","description":"Cytosolic arginine sensor for mTORC1 Subunit 1 (CASTOR1) functions as a key regulator of mechanistic target of rapamycin complex 1 (mTORC1) signaling. Despite its frequent dysregulation in cancers via mechanisms such as KSHV microRNA-mediated inhibition or AKT-driven phosphorylation and degradation, the impact of <i>CASTOR1</i> loss on tumor initiation and progression remains poorly understood. Here, we identify <i>CASTOR1</i> as a critical tumor suppressor in non-small cell lung cancer (NSCLC) by demonstrating that its genetic ablation amplifies tumorigenesis in a <i>KRAS</i>-driven genetically engineered mouse model (GEMM;LSL-<i>KRAS</i> <sup>G12D</sup>). <i>CASTOR1</i> deficiency markedly enhances lung tumor incidence, accelerates tumor progression, and increases proliferative indices i","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-06-30T03:26:21.731Z","creation":"2026-06-30T03:21:01.032Z"},"accession":"S-EPMC12045348","cross_references":{"pubmed":["40313924"],"doi":["10.1101/2025.04.23.650349"]}}