ArticleOncology letters2020
Ubiquitin-specific peptidase 17 promotes cisplatin resistance via PI3K/AKT activation in non-small cell lung cancer.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Ubiquitination and deubiquitination as critical modulators of NSCLC tumorigenesis and drug resistance.Discover oncology · 2026Review
- Article
- A Case Series Exploration of Multi-Regional Expression Heterogeneity in Triple-Negative Breast Cancer Patients.International journal of molecular sciences · 2022Article
- Hypoxic Microenvironment-Induced Reduction in PTEN-L Secretion Promotes Non-Small Cell Lung Cancer Metastasis through PI3K/AKT Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The roles of KLHL family members in human cancers.American journal of cancer research · 2022Review
- The role of the deubiquitinating enzyme DUB3/USP17 in cancer: a narrative review.Cancer cell international · 2021Review
- PI3K/AKT signaling pathway as a critical regulator of Cisplatin response in tumor cells.Oncology research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The suppression of ubiquitin-specific peptidase 17 (USP17) has previously been found to result in reduced tumorigenesis and invasion of non-small cell lung cancer (NSCLC) cells. However, the functions and underlying mechanisms of USP17 in NSCLC progression remain unclear. In the present study, cisplatin treatment was found to upregulate USP17 expression in a dose-dependent manner. Furthermore, USP17-overexpressing (USP17-OE) NSCLC A549 and H1299 cells were generated for mechanistic studies. The results from the Cell Counting Kit-8 assay revealed increased cell proliferation in USP17-OE cells compared with that of control cells. Moreover, the viability of USP17-OE cells was significantly higher than that of the control cells, when treated with cisplatin. The results of the biochemical studies demonstrated enhanced PI3K and AKT phosphorylation in USP17-OE NSCLC cells, whereas USP17-knockdown decreased these levels of phosphorylation. By contrast, an AKT inhibitor abolished the USP17-mediated enhancement of proliferation. Moreover, suppression of USP17 or the combination of the AKT inhibitor and cisplatin significantly reduced cell viability. Overall, the results of the present study suggest that PI3K/AKT activation is the underlying mechanism of USP17-mediated cisplatin resistance in NSCLC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.