Abstract
Breaking Insights| March 15 2023 Highlights from Recent Cancer Literature Author & Article Information Online Issn: 1538-7445 Print Issn: 0008-5472 ©2023 American Association for Cancer Research2023American Association for Cancer Research Cancer Res (2023) 83 (6): 805–806. https://doi.org/10.1158/0008-5472.CAN-83-6-BI 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 March 15 2023 Citation Highlights from Recent Cancer Literature. Cancer Res 15 March 2023; 83 (6): 805–806. https://doi.org/10.1158/0008-5472.CAN-83-6-BI 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 Although the KRAS-protein interactome has been well defined, the functional significance of these protein interactions in KRAS-mutant lung cancer tumorigenesis is poorly understood. Tang and colleagues examined the effect of candidate KRAS-interacting proteins on lung cancer growth utilizing a multiplexed somatic CRISPR/Cas9-based genome editing screen in a KRASG12D mutant mouse model. They found that wild-type HRAS and NRAS suppressed KRAS-driven lung tumorigenesis in vivo and in vitro through suppression of KRAS-KRAS binding as well as through competition for key downstream signaling pathways such as ERK. Expert Commentary: This study suggests that “RAS paralog imbalance” with decreased expression of wild-type HRAS and NRAS in the setting of mutant KRAS can promote tumorigenesis. Tang R, Shuldiner EG, Kelly M, Murray CW, Hebert JD, Andrejka L, et al. Multiplexed screens identify RAS paralogues HRAS and NRAS as suppressors of KRAS-driven lung cancer growth. Nat Cell Biol 2023;25:159-69. Extravasation of metastatic... You do not currently have access to this content.
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