<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang X</submitter><funding>the Fundamental Research Funds for the Central Universities</funding><funding>the Natural Science Foundation of Chongqing, China</funding><funding>Hunan province college students research learning and innovative experiment project</funding><funding>Shandong &amp; Chongqing Science and technology cooperation project</funding><funding>the National Natural Science Foundation of China</funding><funding>Hunan Provincial Health Commission Project</funding><pagination>1798</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11545376</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(21)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Ubiquitination is an important post-transcriptional modification crucial for maintaining cell homeostasis. As a deubiquitination enzyme, ubiquitin-specific protease 1 (USP1) is associated with tumor progression; however, its role in bladder cancer is unknown. This study aimed to analyze USP1 expression and study its roles in bladder cancer.&lt;h4>Methods&lt;/h4>The web server GEPIA was used to analyze the USP1 expression. To explore USP1's function in bladder cancer, we constructed USP1-knockout cell lines in UMUC3 cells. A FLAG-USP1 (WT USP1) plasmid and a plasmid FLAG-USP1 C90S (catalytic-inactive mutant) were used to overexpress USP1 in T24 cells. CCK8, colony formation, and Transwell assays were used to assess cell viability, proliferation, and migration. RNA-sequencing (R</pubmed_abstract><journal>Cells</journal><pubmed_title>Ubiquitin-Specific Protease 1 Promotes Bladder Cancer Progression by Stabilizing c-MYC.</pubmed_title><pmcid>PMC11545376</pmcid><funding_grant_id>CSTB2023TIAD-LDX0029</funding_grant_id><funding_grant_id>202202084830</funding_grant_id><funding_grant_id>CSTB2022NSCQMSX0832</funding_grant_id><funding_grant_id>S202410542176</funding_grant_id><funding_grant_id>81902844，32270760</funding_grant_id><funding_grant_id>2021CDJYGRH-004</funding_grant_id><pubmed_authors>Zhang AQ</pubmed_authors><pubmed_authors>Zhang HH</pubmed_authors><pubmed_authors>Bao LW</pubmed_authors><pubmed_authors>Yu B</pubmed_authors><pubmed_authors>Lei J</pubmed_authors><pubmed_authors>Li T</pubmed_authors><pubmed_authors>Li SZ</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Peng P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ubiquitin-Specific Protease 1 Promotes Bladder Cancer Progression by Stabilizing c-MYC.</name><description>&lt;h4>Background&lt;/h4>Ubiquitination is an important post-transcriptional modification crucial for maintaining cell homeostasis. As a deubiquitination enzyme, ubiquitin-specific protease 1 (USP1) is associated with tumor progression; however, its role in bladder cancer is unknown. This study aimed to analyze USP1 expression and study its roles in bladder cancer.&lt;h4>Methods&lt;/h4>The web server GEPIA was used to analyze the USP1 expression. To explore USP1's function in bladder cancer, we constructed USP1-knockout cell lines in UMUC3 cells. A FLAG-USP1 (WT USP1) plasmid and a plasmid FLAG-USP1 C90S (catalytic-inactive mutant) were used to overexpress USP1 in T24 cells. CCK8, colony formation, and Transwell assays were used to assess cell viability, proliferation, and migration. RNA-sequencing (R</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2025-04-04T14:52:12.583Z</modification><creation>2025-04-04T14:52:12.583Z</creation></dates><accession>S-EPMC11545376</accession><cross_references><pubmed>39513905</pubmed><doi>10.3390/cells13211798</doi></cross_references></HashMap>