The final, formatted version of the article will be published soon.
BRIEF RESEARCH REPORT article
Front. Oncol.
Sec. Cancer Molecular Targets and Therapeutics
Volume 14 - 2024 |
doi: 10.3389/fonc.2024.1456071
Targeted transcriptomic analysis of well-differentiated and dedifferentiated liposarcoma reveals multiple dysregulated pathways including glucose metabolism, TGF-β, and HIF-1 signaling
Provisionally accepted- 1 Wexner Medical Center, The Ohio State University, Columbus, United States
- 2 The James Cancer Hospital and Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, United States
Liposarcoma is the most prevalent sarcoma in adults representing 20% of all sarcomas with welldifferentiated/dedifferentiated among the most common subtypes represented. Despite multimodality treatment approaches, there has not been any appreciable change in survival benefit in the past 10 years. The future of targeted therapy for WD/DDLPS is promising with the intention to spare multi-visceral removal due to radical surgical resection. Therefore, there is a need to expand upon the molecular landscape of WDLPS and DDLPS which can help identify potential therapeutic targets for the treatment of this disease. Targeted transcriptome analysis using the NanoString tumor signaling 360 panel revealed a dysregulation in glucose metabolism and HIF1 signaling pathways in both WDLPS and DDLPS when compared to normal fat controls. WDLPS, however, demonstrated upregulation of HIF-1A and TGF-β when compared to DDLPS by targeted transcriptome analysis and orthogonal validation by RT-qPCR suggesting activation of EMT pathway in WDLPS when compared to DDLPS. Our findings implicate a putative role for dysregulation in glucose metabolism, TGF-β and HIF1 signaling in the pathogenesis of both WD/DDLPS suggesting a possible proinflammatory tumor environment within WDLPS and subsequent activation of the TGF-β signaling pathway.
Keywords: Dedifferentiated liposarcoma, well-differentiated liposarcoma, NanoString, TGF-β, Transcriptome
Received: 27 Jun 2024; Accepted: 16 Oct 2024.
Copyright: © 2024 Patton, Horn, Upadhaya, Sarchet, Pollock, Oghumu and Iwenofu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Obiajulu Hans Iwenofu, Wexner Medical Center, The Ohio State University, Columbus, United States
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.