ArticleBMC cancer2020
Ubiquitin-specific protease-44 inhibits the proliferation and migration of cells via inhibition of JNK pathway in clear cell renal cell carcinoma.
Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- USP52 promotes clear cell renal carcinoma progression by deubiquitinating and stabilizing CORO6.Translational oncology · 2026Article
- Hypermethylated USP44 deubiquitinates SENP2: a critical mechanism in esophageal cancer progression and a new target for intervention.Clinical epigenetics · 2025Article
- Roles of E3 ubiquitin ligases and deubiquitinating enzymes in renal cell carcinoma.Frontiers in oncology · 2025Review
- Detection of differentially methylated CpGs between tumour and adjacent benign cells in diagnostic prostate cancer samples.Scientific reports · 2024Article
- USP44 inactivation accelerates the progression of thyroid cancer by inducing ubiquitylation and degradation of p21.International journal of biological sciences · 2024Article
- The deubiquitinating enzyme USP44 suppresses hepatocellular carcinoma progression by inhibiting Hedgehog signaling and PDL1 expression.Cell death & disease · 2023Article
- The involvement of PDIA2 gene in the progression of renal cell carcinoma is potentially through regulation of JNK signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Targeting the deubiquitinaseOncology reports · 2023Review
- A risk signature of ubiquitin-specific protease family predict the prognosis and therapy of kidney cancer patients.BMC nephrology · 2023Article
- Article
- Extensive intratumor regional epigenetic heterogeneity in clear cell renal cell carcinoma targets kidney enhancers and is associated with poor outcome.Clinical epigenetics · 2023Article
- Bortezomib advanced mechanisms of action in multiple myeloma, solid and liquid tumors along with its novel therapeutic applications.EXCLI journal · 2023Review
- Analysis of mRNA mFrontiers in genetics · 2023Article
- Insight into the physiological and pathological roles of USP44, a potential tumor target (Review).Oncology letters · 2022Review
- USP44 accelerates the growth of T-cell acute lymphoblastic leukemia through interacting with WDR5 and repressing its ubiquitination.International journal of medical sciences · 2022Article
- Lysosomal-Associated Transmembrane Protein 5 Promotes Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma.Journal of oncology · 2022Article
- Landscape of immune cell infiltration in clear cell renal cell carcinoma to aid immunotherapy.Cancer science · 2021Article
- Sohlh2 Inhibits the Malignant Progression of Renal Cell Carcinoma by Upregulating KlothoFrontiers in oncology · 2021Article
- Prognostic Role of the Ubiquitin Proteasome System in Clear Cell Renal Cell Carcinoma: A Bioinformatic Perspective.Journal of Cancer · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundClear cell renal cell carcinoma (ccRCC) is the most common form of adult kidney cancer. Ubiquitin-specific protease (USP)44 has been reported to be involved in various cancers. We investigated the function, role and molecular mechanism of USP44 in ccRCC.
methodsData obtained from the Cancer Genome Atlas Data Portal and Gene Expression Omnibus database were analyzed to uncover the clinical relevance of USP44 expression and tumor development. USP44 function in the proliferation and migration of tumor cells was assessed by cellular and molecular analyses using ccRCC lines (786-O cells and Caki-1 cells).
resultsUSP44 showed low expression in ccRCC cancer tissues compared with that in normal tissue. USP44 expression was negatively correlated with tumor stage, tumor grade, and patient survival. USP44 overexpression inhibited the proliferation and migration of 786-O cells and Caki-1 cells significantly. USP44 overexpression also prohibited cell proliferation by upregulating expression of P21, downregulating cyclin-D1 expression, and inhibiting cell migration by downregulating expression of matrix metalloproteinase (MMP)2 and MMP9. USP44 knockdown enhanced the proliferation and migration of 786-O cells and Caki-1 cells. USP44 function in inhibiting the proliferation and migration of 786-O cells and Caki-1 cells was associated with phosphorylation of Jun N-terminal kinase (JNK).
conclusionUSP44 may be a marker in predicting ccRCC progression. Inhibition by USP44 of the proliferation and migration of 786-O cells and Caki-1 cells is dependent upon the JNK pathway.
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