Exploring GAS5's impact on prostate cancer: Recent discoveries and emerging paradigms
- PMID: 37837861
- DOI: 10.1016/j.prp.2023.154851
Exploring GAS5's impact on prostate cancer: Recent discoveries and emerging paradigms
Abstract
Novel treatment targets must be discovered to improve the results for patients with prostate cancer, which continues to be a significant worldwide health problem. Growth Arrest-Specific 5 (GAS5) is a long non-coding RNA (lncRNA) that has emerged as a promising target. GAS5 is a non-coding RNA that is a tumour suppressor in many different cancers by reducing cell proliferation and increasing apoptosis. GAS5 influences cell cycle control and apoptosis via interactions with important signalling pathways and microRNAs, as has been shown by recent studies. Furthermore, GAS5 has attracted interest for its diagnostic and prognostic potential in prostate cancer. GAS5 expression is a promising biomarker for disease classification and individualized treatment approaches because of its association with clinicopathological characteristics such as tumour stage, Gleason score, and metastatic potential. Preclinical models have revealed encouraging anticancer benefits from experimental techniques employing GAS5 overexpression or synthetic analogues, indicating the possibility of translational treatments. Whether GAS5 can be used as a diagnostic biomarker and therapeutic target might lead to more effective and individualized ways to fight prostate cancer, improving patient outcomes and quality of life. To utilize its potential for therapy and establish it as a useful addition to the clinical arsenal against this pervasive malignancy, more investigation into the complex molecular pathways of GAS5 in prostate cancer is essential. This review highlights the recent advancements and insights into the role of GAS5 in prostate cancer pathogenesis and progression.
Keywords: Cancer; GAS5; LncRNAs; Prostate cancer.
Copyright © 2023 Elsevier GmbH. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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