Selected Articles from This Issue

Abstract

Highlights| October 04 2022 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 (2022) 20 (10): 1469. https://doi.org/10.1158/1541-7786.MCR-20-10-HI Related Content A commentary has been published: Intronic Cis-Element DR8 in hTERT Is Bound by Splicing Factor SF3B4 and Regulates hTERT Splicing in Non–Small Cell Lung Cancer A commentary has been published: Distinct Transcriptional Programs in Ascitic and Solid Cancer Cells Induce Different Responses to Chemotherapy in High-Grade Serous Ovarian Cancer A commentary has been published: TRAF4 Inhibits Bladder Cancer Progression by Promoting BMP/SMAD Signaling View more A commentary has been published: EPAC Regulates Melanoma Growth by Stimulating mTORC1 Signaling and Loss of EPAC Signaling Dependence Correlates with Melanoma Progression 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 October 4 2022 Citation Selected Articles from This Issue. Mol Cancer Res 1 October 2022; 20 (10): 1469. https://doi.org/10.1158/1541-7786.MCR-20-10-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 Cutaneous melanoma metastasis begins with lymphatic invasion, followed by hematogenous dissemination and distant organ metastasis. While Rodríguez, Castro Pérez, Setaluri, and co-authors have shown that exchange protein directly activated by cAMP (EPAC) drives growth and survival in primary melanoma tumors but not metastatic lesions, underlying signaling dynamics remain unclear. In this study, the investigators used genetically matched primary and metastatic melanoma cells and pharmacological and genetic EPAC modulation to query EPAC-regulated signaling in each case. The authors found that a pharmacological EPAC inhibitor, ESI-09, abrogates expression of cyclins, cyclin-dependent kinases (CDK), and CDK inhibitors uniquely in primary melanoma cells, and correspondingly disrupts cell cycle progression only in primary melanoma cells. Mechanistically, the authors demonstrated that while EPAC-mediated RAP1 activation and EPAC subcellular localization are similar in primary and metastatic melanoma cells, EPAC inhibition affects AKT and mTORC1 signaling and downstream metabolic features in primary but not metastatic cells. All together,... You do not currently have access to this content.