Ask about this productRelated genes to: OTUB2 antibody
- Gene:
- OTUB2 NIH gene
- Name:
- OTU deubiquitinase, ubiquitin aldehyde binding 2
- Previous symbol:
- C14orf137
- Synonyms:
- FLJ21916, MGC3102
- Chromosome:
- 14q32.12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-28
- Date modifiied:
- 2015-01-28
Related products to: OTUB2 antibody
Related articles to: OTUB2 antibody
- This study aimed to clarify how cancer-associated fibroblast-derived exosomal circ_0067557 (CAF-exo circ_0067557) promotes epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC) through BHLHE40-mediated transcriptional activation of OTUB2. - Source: PubMed
Publication date: 2026/05/11
Zhang DaoxuZhang JiaqiYang ChengWang YanWang MuhongYu Zhiwei - Colorectal cancer (CRC) is one of the leading causes of cancer-related mortality worldwide. Ferroptosis, an iron-dependent form of programmed cell death, has emerged as a potential therapeutic target. However, the regulatory mechanisms that allow CRC cells to evade ferroptosis are not fully understood. This study focuses on OTUB2, a deubiquitinating enzyme, and its role in stabilizing U2AF2, which allows CRC cells to resist ferroptosis and autophagy. We analyzed CRC cells and clinical samples to evaluate the effects of OTUB2 on U2AF2 deubiquitination. OTUB2 knockdown and overexpression models were established in CRC cell lines (LoVo, RKO, SW480, HT115) to assess ferroptosis and autophagy activity. Various assays, including western blotting, immunoprecipitation, colony formation, and transwell migration assays, were used to evaluate cell proliferation, migration, and iron metabolism markers. In vivo xenograft models were also employed to assess tumor growth under OTUB2-U2AF2 axis disruption. OTUB2 was highly expressed in CRC tissues compared to normal controls. Knockdown of OTUB2 significantly increased ferroptosis, while enhancing autophagy. Conversely, OTUB2 overexpression reduced ferroptosis and autophagy, maintaining CRC cell survival and proliferation. In vivo studies confirmed that disrupting the OTUB2-U2AF2 axis impaired tumor growth by activating both ferroptosis and autophagy. Importantly, a reciprocal activation relationship between ferroptosis and autophagy was observed under OTUB2-U2AF2 axis deficiency. OTUB2 stabilizes U2AF2 in CRC cells, enabling them to evade ferroptosis and autophagy. Disruption of the OTUB2-U2AF2 axis activates both processes, suppressing tumor growth. Targeting this axis presents a promising therapeutic strategy for CRC treatment. - Source: PubMed
Publication date: 2026/05/07
Chen XiQi YanxinNie QigangZhou KaiMo Ao - Docetaxel (DTX) is a standard chemotherapy agent for castration-resistant prostate cancer (CRPC); however, DTX resistance remains a major clinical challenge, and the underlying molecular mechanisms are not fully understood. In our study, it was found that OTUB2 was highly expressed in DTX-resistant CRPC and could be served as a key driver of DTX resistance. Mechanistically, OTUB2 stabilizes the m5C reader ALYREF by removing its K48-linked polyubiquitin chains, leading to increased ALYREF protein levels. And then, ALYREF enhances the mRNA stability and expression of ABCG4, thereby promoting ATP-dependent efflux of DTX. Moreover, the expression of OTUB2 mRNA and protein could be regulated by FOXD3-AS1 derived from cancer-associated fibroblasts (CAFs). More importantly, treatment with OTUB2 inhibitor (OTUB2-IN-1) resensitized resistant CRPC to DTX. Together, our findings establish OTUB2 as a novel driver of DTX resistance in CRPC and highlight the role of CAFs-derived FOXD3-AS1 and OTUB2/ALYREF/ABCG4 axis in modulating DTX resistance of CRPC. - Source: PubMed
Publication date: 2026/03/17
Ke Zhi-BinChen Jia-YinLin BinChen Chao-RanXue Yu-TingSun Jiang-BoYan Zi-HengZhao Yu-XuanLiu Meng-XinWang ZhenXue Xue-YiZheng Qing-ShuiWei YongXu Ning - Gastric cancer (GC) is often diagnosed at an advanced stage due to the absence of early symptoms and low screening rates, resulting in poor prognosis. The progression of GC is closely related to the immune response within the tumor microenvironment (TME). Tumor-associated macrophages (TAMs), particularly the M2 subtype, are the most prevalent inflammatory cells in the TME and play a crucial role in GC. Tumor cells also evade immune surveillance by upregulating CD274. OTUB2, a deubiquitinase, regulates tumor progression by deubiquitinating substrate proteins. However, the role of OTUB2 in TAMs polarization and immune evasion in GC remains unclear. Stable OTUB2 overexpression and knockdown cells were cocultured with M0 macrophages to study TAMs polarization. Flow cytometry was used to analyze M2 TAMs and CD274 expression on GC cells. Cytokine secretion was evaluated by ELISA. T cell killing assays were performed by co-culturing GC cells with CD8 T cells. Co-immunoprecipitation and Western blotting assessed the ubiquitination levels of YAP, TAZ and CD274. In vivo studies were conducted to evaluate OTUB2's effect on TAMs polarization, immune evasion and GC progression. Immunohistochemistry of GC tissues was performed to investigate the correlation between OTUB2 and TME components. OTUB2 overexpression activated YAP/TAZ to increase TGF-β1 and M2 TAMs polarization by inhibiting SMAD7. It also enhanced CD274 expression, promoting immune evasion. OTUB2 deubiquitinated YAP, TAZ, and CD274, preventing their degradation. In vivo, OTUB2 increased M2 TAMs polarization and CD274 expression, exacerbating GC progression. Immunohistochemistry confirmed a positive correlation between OTUB2, M2 TAMs infiltration and CD274 levels and a negative correlation with CD8 T cell infiltration. Kaplan-Meier analysis showed reduced overall survival in GC patients with high OTUB2 expression. OTUB2 promotes M2 TAMs polarization and immune evasion in GC. Targeting OTUB2 offers a promising strategy to reshape the GC TME and improve the efficacy of immune checkpoint inhibitors. - Source: PubMed
Publication date: 2026/04/15
Li JieSun JuanZhang ChenggangHe YixuanZheng ZichengLiu GuanmoLiu YuqinKang WeimingYe Xin - Thyroid collision tumors (TCTs) are rare thyroid malignancies characterized by the coexistence of distinct tumor types. We investigated the histopathology, immunohistochemistry, and gene mutations to comprehensively characterize the heterogeneity of TCTs. - Source: PubMed
Xu YingLi QianLi Mengyu