ArticleThe Kaohsiung journal of medical sciences2019
Ubiquitin specific peptidase 49 inhibits non-small cell lung cancer cell growth by suppressing PI3K/AKT signaling.
Article in The Kaohsiung journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Ubiquitination and deubiquitination as critical modulators of NSCLC tumorigenesis and drug resistance.Discover oncology · 2026Review
- Deubiquitomic and bioinformatic analyses in cisplatin-treated lung cancer cells.International journal of medical sciences · 2026Article
- FBXO2 promotes hepatocellular carcinoma progression and sorafenib resistance by targeting USP49 for proteasomal degradation.Frontiers in immunology · 2025Article
- Genetically predicted effects of 10 sleep phenotypes on revision of knee arthroplasty: a mendelian randomization study.Journal of orthopaedic surgery and research · 2024Article
- The equilibrium of tumor suppression: DUBs as active regulators of PTEN.Experimental & molecular medicine · 2022Review
- Rho family GTPase 1 (RND1), a novel regulator of p53, enhances ferroptosis in glioblastoma.Cell & bioscience · 2022Article
- Fbxo45 facilitates pancreatic carcinoma progression by targeting USP49 for ubiquitination and degradation.Cell death & disease · 2022Article
- Oncogenic Activity of Glucocorticoid Receptor β Is Controlled by Ubiquitination-Dependent Interaction with USP49 in Glioblastoma Cells.Molecular cancer research : MCR · 2022Article
- Knockdown of USP8 inhibits prostate cancer cell growth, proliferation, and metastasis and promotes docetaxel's activity by suppressing the NF-kB signaling pathway.Frontiers in oncology · 2022Article
- miR-5000-3p confers oxaliplatin resistance by targeting ubiquitin-specific peptidase 49 in colorectal cancer.Cell death discovery · 2021Article
- Long non-coding RNA receptor activator of nuclear factor-κ B ligand promotes cisplatin resistance in non-small cell lung cancer cells.Experimental and therapeutic medicine · 2021Article
- Advances in deubiquitinating enzymes in lung adenocarcinoma.Journal of Cancer · 2021Review
- The role of ubiquitination and deubiquitination in cancer metabolism.Molecular cancer · 2020Review
- miR-548b-3p functions as a tumor suppressor in lung cancer.Lasers in medical science · 2020Article
- PTPLAD2 and USP49 Involved in the Pathogenesis of Smoke-Induced COPD by Integrative Bioinformatics Analysis.International journal of chronic obstructive pulmonary disease · 2020Article
- RING Finger Protein 38 Mediates LIM Domain Binding 1 Degradation and Regulates Cell Growth in Colorectal Cancer.OncoTargets and therapy · 2020Article
- Ubiquitin specific peptidase 49 inhibits non-small cell lung cancer cell growth by suppressing PI3K/AKT signaling.The Kaohsiung journal of medical sciences · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Ubiquitin specific peptidase 49 (USP49) has been reported as a tumor suppressor in several tumors, but its function and molecular mechanism in non-small cell lung cancer (NSCLC) are still unknown. In this study, USP49 was found downregulated in NSCLC primary tissues and cell lines, and high USP49 predicted a positive index for the overall survival of NSCLC patients. Overexpression of USP49 downregulated the expression levels of Cyclin D1, and upregulated p53 expression. Further flow cytometry analysis showed that overexpressed USP49 induced cell cycle arrest at G0/G1 phase. As a result, overexpression of USP49 significantly inhibited cell growth of NSCLC cells. In mechanism, overexpression of USP49 inhibited PI3K/AKT signaling, but knockdown of USP49 enhanced this signaling. Further studies indicated that USP49 deubiquitinated PTEN and stabilized PTEN protein, which suggested that USP49 inhibited PI3K/AKT signaling by stabilizing PTEN in NSCLC cells. In conclusion, we demonstrated that USP49 was functional in NSCLC cells, and inhibited NSCLC cell growth by suppressing PI3K/AKT signaling, suggesting that USP49 could be as a novel target for NSCLC therapy.
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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.