Selected Articles from This Issue

Abstract

Highlights| June 01 2023 Selected Articles from This Issue Author & Article Information Online ISSN: 1557-3125 Print ISSN: 1541-7786 ©2023 American Association for Cancer Research2023American Association for Cancer Research Mol Cancer Res (2023) 21 (6): 495. https://doi.org/10.1158/1541-7786.MCR-21-6-HI Related Content A commentary has been published: Interdependence of SS18-SSX–driven YAP1 and β-Catenin Activation in Synovial Sarcoma A commentary has been published: USP10 Regulates ZEB1 Ubiquitination and Protein Stability to Inhibit ZEB1-Mediated Colorectal Cancer Metastasis A commentary has been published: UBE2C-mediated Autophagy Inhibition via Ubiquitination of SIRT1 Contributes to Endometrial Cancer Progression View more A commentary has been published: Targeting Unc51-like Autophagy Activating Kinase 1 (ULK1) Overcomes Adaptive Drug Resistance in Acute Myelogenous Leukemia View less Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record June 1 2023 Citation Selected Articles from This Issue. Mol Cancer Res 1 June 2023; 21 (6): 495. https://doi.org/10.1158/1541-7786.MCR-21-6-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 Synovial sarcoma arises from a reciprocal t(X;18)(p11;q11) translocation and resulting SS18-SSX fusion protein, which integrates into the BAF chromatin remodeling complex and dysregulates global transcription. While YAP and β-catenin are known SS18-SSX targets, whether YAP/β-catenin crosstalk occurs is not known. Using YAP and β-catenin genetic depletion and pharmacologic inhibition alongside reporters for each transcriptional coactivator in synovial sarcoma cell lines, Isfort and colleagues found that YAP and β-catenin mutually enhance each other's activity. Furthermore, the authors demonstrated that YAP/β-catenin coactivation occurs exclusively in SS18-SSX–expressing synovial sarcoma cell lines, and that abrogating SS18-SSX expression using siRNA eliminates YAP/β-catenin crosstalk. siRNA-mediated BAF complex component ablation also inhibits YAP/β-catenin coactivation, demonstrating that the SS18-SSX–containing BAF complex is required for YAP/β-catenin crosstalk. In sum, this study presents YAP/β-catenin coactivation as a SS18-SSX–driven transcriptional phenomenon that may represent a unique therapeutic vulnerability in synovial sarcoma. While targeted therapies provide efficacy against acute myelogenous leukemia (AML),... You do not currently have access to this content.