{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xu LM"],"funding":["the National Natural Science Foundation of China"],"pagination":["350"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9344728"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(1)"],"pubmed_abstract":["<h4>Background</h4>The resistance to radiotherapy remains a major obstacle that limits the efficacy of radiotherapy in non-small cell lung cancer (NSCLC). This study aims to illustrate the molecular mechanism underlying the role of LINC00665 in the radiosensitivity of NSCLC, which involves ubiquitin C-terminal hydrolase L3 (UCHL3).<h4>Methods and results</h4>The expression of UCHL3 was determined in clinical tissue samples collected from NSCLC patients and NSCLC cell lines. We found that UCHL3 overexpression occurred in both NSCLC tissues and cells, associated with poor prognosis in NSCLC patients. Mechanistically, UCHL3 stabilized aryl hydrocarbon receptor (AhR) protein through deubiquitination, thereby promoting PD-L1 expression. UCHL3 reduced the radiosensitivity of NSCLC cells by stabi"],"journal":["Journal of translational medicine"],"pubmed_title":["LINC00665 knockdown confers sensitivity in irradiated non-small cell lung cancer cells through the miR-582-5p/UCHL3/AhR axis."],"pmcid":["PMC9344728"],"funding_grant_id":["No. 81502656","No. 81501140"],"pubmed_authors":["Yuan YJ","Wang P","Wang S","Xu LM","Yu H"],"additional_accession":[]},"is_claimable":false,"name":"LINC00665 knockdown confers sensitivity in irradiated non-small cell lung cancer cells through the miR-582-5p/UCHL3/AhR axis.","description":"<h4>Background</h4>The resistance to radiotherapy remains a major obstacle that limits the efficacy of radiotherapy in non-small cell lung cancer (NSCLC). This study aims to illustrate the molecular mechanism underlying the role of LINC00665 in the radiosensitivity of NSCLC, which involves ubiquitin C-terminal hydrolase L3 (UCHL3).<h4>Methods and results</h4>The expression of UCHL3 was determined in clinical tissue samples collected from NSCLC patients and NSCLC cell lines. We found that UCHL3 overexpression occurred in both NSCLC tissues and cells, associated with poor prognosis in NSCLC patients. Mechanistically, UCHL3 stabilized aryl hydrocarbon receptor (AhR) protein through deubiquitination, thereby promoting PD-L1 expression. UCHL3 reduced the radiosensitivity of NSCLC cells by stabi","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2025-04-26T12:04:32.291Z","creation":"2025-02-19T05:06:05.352Z"},"accession":"S-EPMC9344728","cross_references":{"pubmed":["35918714"],"doi":["10.1186/s12967-022-03516-2"]}}