ArticleCancer medicine2025
USP15 Drives NSCLC Progression and Chemoresistance, Potentially via Regulation of the U2-Type Spliceosomal Complex.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- USP15 regulates mitotic fidelity, metastatic potential, and chemotherapeutic response in ovarian cancer cells.Molecular therapy. Oncology · 2026Article
- USP15 Drives NSCLC Progression and Chemoresistance, Potentially via Regulation of the U2-Type Spliceosomal Complex.Cancer medicine · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
objectiveNon-small cell lung cancer (NSCLC) is an aggressive and lethal malignancy with the highest cancer-related mortality rate. More than 50% of patients are diagnosed at advanced stages, often accompanied by chemoresistance and poor prognosis. Deubiquitinases (DUBs), which regulate various signaling pathways by removing ubiquitin moieties, are frequently dysregulated in tumors, including the ubiquitin-specific processing protease 15 (USP15). However, the biological role of USP15 in NSCLC progression remains poorly defined. This study aimed to investigate the biological function and mechanistic relevance of USP15 in NSCLC.
methodUSP15 expression in human NSCLC tumor tissues and matched adjacent normal tissues was assessed by immunohistochemical staining. Western blotting was performed to evaluate USP15 protein levels in various NSCLC cell lines. Functional assays were conducted to examine the effects of USP15 knockdown on NSCLC cell growth, invasion, and epithelial-mesenchymal transition (EMT). Chemosensitivity assays were carried out using topotecan and irinotecan. Additionally, proteomic analysis was performed through immunoprecipitation of tGFP-tagged USP15 followed by LC-MS/MS to identify USP15-interacting proteins.
resultsUSP15 was significantly overexpressed in NSCLC tumor tissues compared to adjacent normal tissues, as confirmed by immunohistochemistry. This finding was further supported by western blot analysis showing elevated USP15 levels across multiple NSCLC cell lines. Knockdown of USP15 impaired NSCLC cell growth and invasion, reduced EMT marker expression, and re-sensitized cells to topotecan and irinotecan. Proteomic profiling identified USP15-interacting proteins enriched in the U2-type spliceosomal complex and RNA helicase activity, suggesting a role for USP15 in regulating pre-mRNA splicing. DISCUSSION: This study demonstrates the oncogenic role of USP15 in NSCLC, highlighting its contribution to tumor progression, chemoresistance, and RNA processing. The findings provide mechanistic insights into how USP15 may drive NSCLC pathogenesis through modulation of spliceosome-associated proteins. These results support the potential of USP15 as both a diagnostic biomarker and a therapeutic target in NSCLC.
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