Ask about this productRelated genes to: UBE2S antibody
- Gene:
- UBE2S NIH gene
- Name:
- ubiquitin conjugating enzyme E2 S
- Previous symbol:
- -
- Synonyms:
- E2-EPF
- Chromosome:
- 19q13.43
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-12
- Date modifiied:
- 2016-03-14
Related products to: UBE2S antibody
Related articles to: UBE2S antibody
- This study aims to investigate the biological function, molecular mechanisms, and impact on the tumor microenvironment of the ubiquitin-conjugating enzyme E2S (UBE2S) in the progression of kidney renal clear cell carcinoma (KIRC). Based on the TCGA and GEPIA databases, the relationship between UBE2S expression and patient prognosis was analyzed. Overexpression and knockdown models of UBE2S were established in Caki-1 and 786-O cell lines. Cell proliferation, apoptosis, and migration capabilities were assessed using CCK-8 assay, colony formation assay, flow cytometry, wound healing assay, and Transwell assay. Protein-protein interactions and expression regulatory mechanisms were validated by co-immunoprecipitation and Western blot. The proteasome inhibitor MG132 and ubiquitination assays were employed to investigate protein degradation mechanisms. Macrophage polarization was analyzed using a cell co-culture system, immunofluorescence staining, and Western blot. UBE2S is highly expressed in KIRC tissues and is associated with poor patient prognosis. Functional experiments demonstrate that UBE2S promotes KIRC cell proliferation and migration while inhibiting apoptosis. Mechanistically, UBE2S directly binds to and positively regulates CDC20 protein expression, and its oncogenic functions depend on CDC20. Furthermore, knockdown of UBE2S induces cuproptosis by activating FDX1 protein, thereby enhancing cellular sensitivity to cuproptosis inducers. UBE2S promotes FDX1 protein degradation via the ubiquitin-proteasome pathway. Additionally, tumor cells with high UBE2S expression promote macrophage polarization toward the M2 phenotype. UBE2S drives KIRC progression by regulating CDC20 expression and suppressing FDX1-mediated cuproptosis, thereby promoting tumor-associated macrophage polarization. - Source: PubMed
Publication date: 2026/08/30
Chen JunruGao YuFeng YuelongYang HaoJia GangWei JiaoZhang LingxiaZhang Zhizhong - Uveal melanoma (UM) is a challenging malignancy, in terms of diagnosis, risk stratification, and treatment associated with high morbidity and mortality rates. It has been demonstrated that E2F-related pathways play a significant role in the tumorigenesis and distant metastasis of UM. In this study, the E2F target-related genes were utilized to construct and validate a prognostic risk score for patients with UM. - Source: PubMed
Publication date: 2026/05/14
Al Sharie Ahmed HTashtoush Mais BDarweesh Reem FJadallah Rand KAl-Karaki Jawad MAl-Omari Samah OAleshawi Abdelwahab JAlqudah Asem AAlemam AmerAbu Serhan HashemElnahry Ayman GEl-Elimat TamamAl-Dwairi Rami - Clear cell renal cell carcinoma (ccRCC) is highly heterogeneous, and robust biomarkers for risk stratification and therapeutic guidance remain limited. - Source: PubMed
Publication date: 2026/05/14
Leng KangZhou YihengZhao JianWang XiaoguangSong Hua - BACKGROUND: Small cell lung cancer (SCLC) is a highly aggressive neuroendocrine malignancy characterized by rapid progression and poor survival. While the ubiquitin-conjugating enzyme E2 S (UBE2S) has been investigated in non-small cell lung cancer (NSCLC), its expression, functional roles, and underlying mechanisms in SCLC remain largely undefined. This study aims to elucidate the contribution of UBE2S to SCLC pathogenesis, metabolic reprogramming, and cellular plasticity. METHODS: UBE2S expression was analyzed using public databases (TCGA, GEO, LinkedOmics, TIMER, UALCAN, etc.) and validated by immunohistochemistry on lung cancer tissue microarrays. Gain- and loss-of-function experiments were conducted in SCLC cell lines. Multi-omics approaches—including single-cell RNA sequencing (scRNA-seq), proteomics, metabolomics, and immunoprecipitation-mass spectrometry (IP-MS)—were employed. Virtual screening was performed against the UBE2S structure to identify potential inhibitors. Statistical significance was assessed using Student’s t-test, ANOVA or adjusted p-values as appropriate. RESULTS: UBE2S was significantly upregulated in SCLC compared to NSCLC, with protein levels escalating from lung squamous cell carcinoma (LUSC) to lung adenocarcinoma (LUAD) to SCLC. Elevated UBE2S expression correlated with advanced stage in both LUAD and SCLC. Functional studies in vitro and in vivo demonstrated that UBE2S promotes SCLC proliferation and cell cycle progression by driving G1/S transition. ScRNA-seq revealed specific enrichment of UBE2S in SCLC cells and implicated it in NSCLC-to-SCLC phenotypic plasticity. Integrated proteomic and metabolomic analyses indicated that UBE2S remodels metabolism, activating pathways such as folate and amino acid biosynthesis. IP-MS identified the transcription factor DLX6 as a novel UBE2S interactor, with UBE2S overexpression reducing DLX6 protein stability. Virtual screening integrated with functional assays identified Odetiglucan as a selective proliferation inhibitor for UBE2S-high cells. CONCLUSIONS: UBE2S drives SCLC malignant progression by regulating cell cycle and metabolic reprogramming, mediated in part through its interaction with DLX6. Odetiglucan, with its documented immunomodulatory functions, represents a promising therapeutic candidate for SCLC with high UBE2S expression. Our findings establish UBE2S as a key oncoprotein and potential therapeutic target in SCLC. - Source: PubMed
Publication date: 2026/04/24
Yan XiaodongPan ShouqiangZhang JinMao KeleiYu RuihaoXiong YiduoHuang HaixiaZhang Yi - Lung adenocarcinoma (LUAD) is the predominant pathological subtype of non-small cell lung cancer. Its considerable tumor heterogeneity and drug resistance present major clinical obstacles, resulting in unfavorable patient outcomes. Protein palmitoylation is known to be a key factor in tumorigenesis; however, its cell-specific expression patterns and prognostic value in LUAD remain incompletely characterized. - Source: PubMed
Publication date: 2026/04/06
Liu HaixiaoHu YueWang LingyunLi ChanglinLi DongtaoMeng LinghanZheng GuangdaRen JuanxiaShang LuBao Yanju