Ubiquitin specific peptidases and prostate cancer

Guo, Yunfei; Cui, Shuaishuai; Chen, Yuanyuan; Guo, Song; Chen, Dahu

doi:10.7717/peerj.14799

Cited by 9 publications

(8 citation statements)

References 128 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In prokaryotes, ClpP and Lon are the major proteasomes that participate in the proximal ATP-dependent steps of substrate degradation [ 10 ]. UPS participates in intracellular protein proteasome-dependent degradation, cell metabolism, cell cycle progression, chromosome separation, kinase activation, apoptosis, DNA repair, and so on [ 11 , 12 , 13 ]. Ubiquitination modification is a primary mode of intracellular protein degradation in eukaryotes mediated by ubiquitin; it is initiated by enzyme E1 (ubiquitin-activating enzyme), which generates thioester bonds between its Cys residue and the ubiquitin C terminus using ATP-dependent hydrolysis.…”

Section: Introductionmentioning

confidence: 99%

The Ubiquitin–Proteasome System in Tumor Metabolism

Wang

Xiang

Fan

et al. 2023

Cancers

View full text Add to dashboard Cite

Metabolic reprogramming, which is considered a hallmark of cancer, can maintain the homeostasis of the tumor environment and promote the proliferation, survival, and metastasis of cancer cells. For instance, increased glucose uptake and high glucose consumption, known as the “Warburg effect,” play an essential part in tumor metabolic reprogramming. In addition, fatty acids are harnessed to satisfy the increased requirement for the phospholipid components of biological membranes and energy. Moreover, the anabolism/catabolism of amino acids, such as glutamine, cystine, and serine, provides nitrogen donors for biosynthesis processes, development of the tumor inflammatory environment, and signal transduction. The ubiquitin–proteasome system (UPS) has been widely reported to be involved in various cellular biological activities. A potential role of UPS in the metabolic regulation of tumor cells has also been reported, but the specific regulatory mechanism has not been elucidated. Here, we review the role of ubiquitination and deubiquitination modification on major metabolic enzymes and important signaling pathways in tumor metabolism to inspire new strategies for the clinical treatment of cancer.

show abstract

Section: Introductionmentioning

confidence: 99%

The Ubiquitin–Proteasome System in Tumor Metabolism

Wang

Xiang

Fan

et al. 2023

Cancers

View full text Add to dashboard Cite

show abstract

“…It has been found that changes in the ubiquitin system may lead to the occurrence of human diseases (Mooney & Sahingur, 2021). Ubiquitinated degradation of genes is a widespread posttranslational modification that plays an important biological regulatory role in cells (Guo et al., 2023; Qin et al., 2022). Studies had shown that USP47 could directly stabilize BACH1 to enhance NSCLC tumor growth by deubiquitination (Peng et al., 2022).…”

Section: Discussionmentioning

confidence: 99%

Icariin promotes osteogenic differentiation of human bone marrow mesenchymal stem cells by regulating USP47/SIRT1/Wnt/β‐catenin

Wang,

Zhang,

Zhang

et al. 2024

Chem Biol Drug Des

View full text Add to dashboard Cite

Icariin has been shown to promote osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). However, the underlying molecular mechanism by which Icariin regulates osteogenic differentiation needs to be further revealed. The viability of BMSCs was assessed by cell counting kit 8 assay. BMSC osteogenic differentiation ability was evaluated by detecting alkaline phosphatase activity and performing alizarin red S staining. The protein levels of osteogenic differentiation‐related markers, sirtuin 1 (SIRT1), ubiquitin‐specific protease 47 (USP47), and Wnt/β‐catenin‐related markers were determined using western blot. SIRT1 mRNA level was measured using quantitative real‐time PCR. The regulation of USP47 on SIRT1 was confirmed by ubiquitination detection and co‐immunoprecipitation analysis. Icariin could promote BMSC osteogenic differentiation. SIRT1 expression was enhanced by Icariin, and its knockdown suppressed Icariin‐induced BMSC osteogenic differentiation. Moreover, deubiquitinating enzyme USP47 could stabilize SIRT1 protein expression. Besides, SIRT1 overexpression reversed the inhibiting effect of USP47 knockdown on BMSC osteogenic differentiation, and USP47 knockdown also restrained Icariin‐induced BMSC osteogenic differentiation. Additionally, Icariin enhanced the activity of the Wnt/β‐catenin pathway by upregulating SIRT1. Icariin facilitated BMSC osteogenic differentiation via the USP47/SIRT1/Wnt/β‐catenin pathway.

show abstract

“…Ubiquitination is involved in the regulation of various protein functions including cell proliferation, cell cycle, DNA damage repair and transmembrane transportation by the regulation of ubiquitin and deubiquitination enzymes (DUBs), among which ubiquitin speci c peptidases (USPs) play the most signi cant role [34]. Each ubiquitin molecule is contained by seven lysine (K) residues (K6, K11, K27, K29, K33, K48, and K63), as well be assembled into eight types of ubiquitin chain linkages through covalently conjugating the C-terminal glycine of a second ubiquitin molecule with one of the seven lysine residues or the aminoterminal methionine (Met1) on the rst ubiquitin moiety.…”

Section: Discussionmentioning

confidence: 99%

Expression, Prognostic and Immunological Roles of USP8 in kidney renal clear cell carcinoma: An Integrated Analysis

Yan,

Yue,

Qiying

et al. 2024

Preprint

View full text Add to dashboard Cite

Background USP8 is a deubiquitinating enzymes (DUBs) that belongs to the ubiquitin-specific processing (USP) protease family. Previous study revealed that USP8 overexpressed and acted as oncogenes in multiple cancers. However, the function of USP8 in kidney renal clear cell carcinoma (KIRC) remains unclear. This research aimed to investigate USP8 expression, prognostic value and its possible roles in tumor immunity in KIRC. Methods Data on patients diagnosed with KIRC were extracted from the TCGA-KIRC and other public omics databases. We detected the expression profiles, clinical relevance and diagnostic value of USP8 in KIRC using GEPIA, UALCAN, GTEx, TIMER, Kaplan-Meier Plotter and HPA Database. The epigenetic characteristics of USP8 were detected by UALCAN and DNMIVD Database. Co-expressed with USP8 and related mechanism analyses were conducted by retrieving data in STRING and cBioPortal. In addition, immune infiltration, single-cell expression and immunotherapy-related analyses were performed by TIMER and TISCH2. Results Low expression levels of USP8 were observed in most cancer types. USP8 mRNA and proteins were downregulated in KIRC. Detection of epigenetics and genetics of USP8 suggested that its expression was negatively related to DNA methylation. Higher-expressed USP8 patients had a better prognosis, including overall survival (OS) and disease free survival (DFS). USP8 mRNA was aberrantly downregulated and correlated to sample types, tumor grade, stages, subtypes and nodal status. Immune infiltration and single-cell analysis suggested the indispensable role of USP8 expression in immune cell infiltration, indicating that USP8 may be an underlying predictor of immune treatment effects for KIRC patients. Meanwhile, the USP8-related gene expression signature in KIRC is correlated to the enrichment of genes involved in the ErbB signaling pathway, Ubiquitin mediated proteolysis, EGFR tyrosine kinase inhibitor resistance, etc. Conclusions Methylated USP8 may act as a novel prognostic and immunotherapy biomarker for KIRC.

show abstract

Ubiquitin specific peptidases and prostate cancer

Cited by 9 publications

References 128 publications

The Ubiquitin–Proteasome System in Tumor Metabolism

The Ubiquitin–Proteasome System in Tumor Metabolism

Icariin promotes osteogenic differentiation of human bone marrow mesenchymal stem cells by regulating USP47/SIRT1/Wnt/β‐catenin

Expression, Prognostic and Immunological Roles of USP8 in kidney renal clear cell carcinoma: An Integrated Analysis

Contact Info

Product

Resources

About