Selected Articles from This Issue

Abstract

Highlights| January 03 2023 Selected Articles from This Issue Author & Article Information Online Issn: 1557-3125 Print Issn: 1541-7786 ©2022 American Association for Cancer Research2022American Association for Cancer Research Mol Cancer Res (2023) 21 (1): 1. https://doi.org/10.1158/1541-7786.MCR-21-1-HI Related Content A commentary has been published: Subtype and Site Specific–Induced Metabolic Vulnerabilities in Prostate Cancer A commentary has been published: GSTA4 Governs Melanoma Immune Resistance and Metastasis A commentary has been published: Mitochondrial Aconitase ACO2 Links Iron Homeostasis with Tumorigenicity in Non–Small Cell Lung Cancer View more A commentary has been published: JAZF1: A Metabolic Regulator of Sensitivity to a Polyamine-Targeted Therapy View less Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record January 3 2023 Citation Selected Articles from This Issue. Mol Cancer Res 1 January 2023; 21 (1): 1. https://doi.org/10.1158/1541-7786.MCR-21-1-HI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search While several non-small cell lung cancer (NSCLC) oncogenic drivers have been identified and therapeutically targeted, many patients harbor aggressive NSCLC tumors lacking targetable oncogenic drivers. Patient-derived xenograft (PDX) models provide useful resources for novel oncogenic driver discovery, as PDX engraftment in immunocompromised mice is a prognostic indicator of poor disease outcomes. By defining engrafting and non-engrafting NSCLC proteomes using mass spectrometry, Mirhadi and colleagues discovered that engrafting tumors exhibit low mitochondrial aconitase (ACO2) and intracellular labile iron levels. Overexpressing ACO2 limits tumor growth in vivo and abrogating its expression using inducible shRNA enhances colony formation in vitro, underscoring the role of ACO2 as a tumor suppressor in NSCLC. Mechanistically, the authors found that ACO2-isocitrate dehydrogenase (IDH) reaction-generated NADPH inhibits mitoNEET (mNT), which could activate iron response element binding protein 1 (IRP1) to facilitate transferrin receptor stabilization and subsequent iron uptake. Correspondingly, iron supplementation or mNT inhibition using pioglitazone hydrochloride... You do not currently have access to this content.