Deciphering the Role of USP16 in Lung Cancer

first_page Download PDF settings Order Article Reprints Font Type: Arial Georgia Verdana Font Size: Aa Aa Aa Line Spacing:    Column Width:    Background: Open AccessAbstract Deciphering the Role of USP16 in Lung Cancer † by Valentina SerratoreValentina Serratore SciProfiles Scilit Preprints.org Google Scholar , Carmen Di RuoccoCarmen Di Ruocco SciProfiles Scilit Preprints.org Google Scholar , Annamaria CerantonioAnnamaria Cerantonio SciProfiles Scilit Preprints.org Google Scholar , Carmela De MarcoCarmela De Marco SciProfiles Scilit Preprints.org Google Scholar * and Giuseppe VigliettoGiuseppe Viglietto SciProfiles Scilit Preprints.org Google Scholar Department of Experimental and Clinical Medicine, "Magna Graecia" University of Catanzaro, 88100 Catanzaro, Italy * Author to whom correspondence should be addressed. † Presented at the 4th International Electronic Conference on Cancers, 6–8 March 2024; Available online: https://sciforum.net/event/IECC2024. Proceedings 2024, 100(1), 17; https://doi.org/10.3390/proceedings2024100017 Published: 27 March 2024 Download keyboard_arrow_down Download PDF Download PDF with Cover Download XML Download Epub Versions Notes Keywords: lung cancer; USP16; DNA repair; cytotoxicity Deubiquitylating enzymes are proteases that reverse the ubiquitination of proteins, an important process for maintaining normal homeostasis.USP16 is a deubiquitylating enzyme that belongs to the family of ubiquitin-specific proteases (USPs) and is involved in cell cycle progression and chromatin remodeling.To elucidate the role of USP16 in lung cancer progression, we first analyzed its expression in a cohort of biopsies obtained from patients with non-small cell lung cancer, NSCLC (N = 18). Real-time PCR analysis and Western blot analysis showed that USP16 is highly expressed in NSCLC tissues compared to normal tissues. To characterize the role of USP16, we used two lung cancer cell lines (NCI-H460 and A549), in which USP16 was knocked down by lentiviral RNA interference (shUSP16).The knockdown of USP16 affects cancer cell behavior in terms of proliferation and drug sensitivity. The knockdown of USP16 reduces the proliferation of cancer cells (≈40%) compared to control cells, which is due to defects in mitotic cell phase. These effects could be attributed to the deubiquitinating effect on its substrates. Indeed, the silencing of USP16 decreased the protein stability of the transcription factor Myc and Polo like kinase-1 (PLK1). Conversely, we found that USP16 impaired the response of lung cancer cells to platinum-containing compounds. The reduction of USP16 expression impairs the cytotoxicity of cisplatin by approximately 50% compared to control cells. This could likely be due to the impaired recruitment of repair proteins in proximity of double-strand breaks (DSBs) in lung cancer cells. These results prompted us to perform further analysis to investigate the role of USP16 in DNA repair and drug sensitivity. Author ContributionsConceptualization, C.D.M. and G.V.; methodology, C.D.M. and V.S.; validation, V.S.; formal analysis, V.S. and C.D.M.; investigation, V.S., C.D.R. and A.C.; resources, C.D.M.; data curation, V.S. and C.D.M.; writing—original draft preparation, V.S. and C.D.M.; writing—review and editing, C.D.M.; visualization, V.S. and C.D.M.; supervision, C.D.M. and G.V.; project administration, C.D.M. and G.V.; funding acquisition, G.V. All authors have read and agreed to the published version of the manuscript.FundingThis work wa salso supported by grants from Ministero dell'Istruzione, dell'Università e della Ricerca (MIUR) to G. Viglietto (20209KY3Y7_003).Institutional Review Board StatementThe study was conducted in accordance with the Declaration of Helsinki, and approved by the internal Review Board of the AOU Mater Domini/University Magna Graecia (Catanzaro, Italy) in the meeting of 16 March 2011.Informed Consent StatementWritten informed consent was obtained from all participants to the study.Data Availability StatementNot applicable.Conflicts of InterestThe authors declare no conflict of interest.Disclaimer/Publisher's Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content. © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Share and Cite MDPI and ACS Style Serratore, V.; Di Ruocco, C.; Cerantonio, A.; De Marco, C.; Viglietto, G. Deciphering the Role of USP16 in Lung Cancer. Proceedings 2024, 100, 17. https://doi.org/10.3390/proceedings2024100017 AMA Style Serratore V, Di Ruocco C, Cerantonio A, De Marco C, Viglietto G. Deciphering the Role of USP16 in Lung Cancer. Proceedings. 2024; 100(1):17. https://doi.org/10.3390/proceedings2024100017 Chicago/Turabian Style Serratore, Valentina, Carmen Di Ruocco, Annamaria Cerantonio, Carmela De Marco, and Giuseppe Viglietto. 2024. "Deciphering the Role of USP16 in Lung Cancer" Proceedings 100, no. 1: 17. https://doi.org/10.3390/proceedings2024100017 Article Metrics No No Article Access Statistics Multiple requests from the same IP address are counted as one view.