AIB1 Monoclonal Antibody [50B6]
- Known as:
- AIB1 Monoclonal Antibody [50B6]
- Catalog number:
- A-0424-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- AIB1 Monoclonal Antibody [50B6]
Related genes to: AIB1 Monoclonal Antibody [50B6]
- Gene:
- NCOA3 NIH gene
- Name:
- nuclear receptor coactivator 3
- Previous symbol:
- -
- Synonyms:
- RAC3, AIB1, ACTR, p/CIP, TRAM-1, CAGH16, TNRC16, KAT13B, bHLHe42, SRC-3, SRC3
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2016-10-05
Related products to: AIB1 Monoclonal Antibody [50B6]
Related articles to: AIB1 Monoclonal Antibody [50B6]
- Triple-negative breast cancer (TNBC) exhibits aggressive biology and heterogeneous immune infiltration. Lysine-specific demethylase 1 (LSD1/KDM1A) is an epigenetic regulator implicated in oncogenic transcriptional programs, but its role in immune exclusion remains incompletely defined. LSD1 expression was evaluated by immunohistochemistry in TNBC specimens and correlated with survival. Functional effects of LSD1 depletion or pharmacological inhibition were assessed in TNBC cell lines and patient-derived xenograft organoids (PDXOs). Transcriptomic, ChIP-seq, multiplex immunofluorescence, and GeoMX digital spatial profiling analyses were integrated to characterize LSD1-associated transcriptional, chromatin, and immune programs. PBMC-PDXO co-cultures evaluated the effects of LSD1 inhibition on tumor growth and immune cell infiltration. High LSD1 expression was associated with inferior overall survival, hypoxia-associated programs and suppressed immune pathways. LSD1-high tumors exhibited reduced infiltration of T cells, B cells, NKT-like cells, and macrophages. Spatial profiling revealed suppressed innate immune responses and type I interferon signaling within B-cell and T-cell compartments, respectively. ChIP-seq demonstrated preferential LSD1 occupancy at AP-1 motif-enriched regions, while co-immunoprecipitation supported association with AP-1 complexes. Integration of LSD1 chromatin occupancy sites with transcriptomics data identified and as candidate LSD1-regulated genes associated with interferon-γ response pathways. LSD1 depletion increased SPPL2A, NCOA3, MHC-I and PD-L1 expression. LSD1 inhibition reduced PDXO growth and increased immune cell infiltration. LSD1 is associated with a poor clinical outcome and immune exclusion in TNBC. These findings support a role for LSD1 in AP-1-associated chromatin regulation and interferon-γ-related transcriptional response; they warrant further investigation into LSD1 inhibition as a therapeutic strategy for immune-cold TNBCs. - Source: PubMed
Publication date: 2026/09/09
Lee Dong YeulHong Jing HanGuan PeiyongLee BernettCui JianzhouLau Hui XinYeong Joe Poh ShengTan Puay HoonChen JinmiaoTeh Bin TeanIqbal Jabed - Spindle cell/sclerosing rhabdomyosarcoma (SRMS) comprises a heterogeneous group of tumors characterized by distinct molecular alterations and clinical behaviors. Among them, ZFP64::NCOA3 fusion-positive SRMS represents an extremely rare subtype, and its biological characteristics remain poorly understood because of the lack of representative experimental models. In this study, we established a patient-derived organoid (PDO) line, designated OICI-RMS-1275, together with organoid-derived xenograft (ODX) models from a previously reported case of ZFP64::NCOA3 fusion-positive SRMS using a modified air-liquid interface organoid culture method. The established organoids exhibited stable long-term propagation and retained tumorigenic capacity following serial transplantation into NOD-scid IL2Rgnull mice. Histological and immunohistochemical analyses demonstrated preservation of the characteristic spindle cell morphology and diffuse expression of MyoD1 and PAX7 observed in the original tumor. Polymerase chain reaction and Sanger sequencing confirmed retention of the ZFP64::NCOA3 fusion transcript and fusion breakpoint in the organoids and ODXs. Lentiviral-mediated knockdown of the fusion gene significantly suppressed organoid proliferation, indicating dependency on ZFP64::NCOA3 for tumor growth. Transcriptomic analyses revealed preservation of major transcriptional features between the original tumor and ODXs, including myogenic lineage-associated gene expression programs. Fusion-gene suppression decreased expression of MYOD1 and DLK1 while increasing PPARG expression, suggesting involvement of the fusion in lineage-associated transcriptional regulation. Under adipogenic induction conditions, SRMS organoids exhibited lipid accumulation detected by Oil Red O staining regardless of fusion-gene suppression status, indicating preserved adipogenic differentiation potential. These findings establish the first PDO and ODX models of ZFP64::NCOA3 fusion-positive SRMS and demonstrate fusion-gene dependency in this rare molecular subtype. Our results further suggest that despite strong myogenic transcriptional programs, fusion-positive SRMS retains adipogenic differentiation capacity. These models provide a valuable platform for investigating disease biology and developing novel therapeutic strategies for rare fusion-positive rhabdomyosarcomas. - Source: PubMed
Publication date: 2026/08/20
Miyamoto RyotaYoshida KeiichiMatsuoka YukikoSasagawa SatoruNagamine NorikoKukita YojiSabe HideakiYoshimura YusukeTakami HarunaSuzuki RieTamiya HironariKakunaga ShigekiImura YoshinoriNakai ShoOkada SeijiYagi ToshinariYoshida Ken-IchiTakenaka SatoshiWakamatsu Toru - Angiofibroma of soft tissue (AFST) is a rare benign fibroblastic/myofibroblastic neoplasm. Despite several published studies describing the clinicopathological features of AFSTs, its cytological characteristics remain poorly documented. This study aimed to identify distinctive cytological features that may support accurate diagnosis. - Source: PubMed
Ito TakahikoYamashita KyokoIkebata KoichiBaba SatokoTogashi YukiDobashi AkitoAe KeisukeMatsumoto SeiichiTakeuchi KengoAbe HitoshiChiba Tomohiro - Approximately 60% of patients with ulcerative colitis (UC) show steroid resistance or dependence, underscoring the need for biomarkers predicting therapeutic response. Despite increasing availability of biologics, corticosteroids remain essential first-line therapy for moderate-to-severe flares in many settings. We applied an integrative systems biology and machine-learning framework to combine microRNA (miR) and mRNA expression profiles from matched rectal biopsies and plasma samples of UC patients treated with corticosteroids, aiming at exploring classification potential of such biological data. Transcriptomic mRNA and miR profiling was performed at baseline and after three days of therapy, and patients were classified as responders or non-responders after seven days. Differential expression results were embedded into a previously defined curated molecular network-based mathematical model of the mechanism of action (MoA) of glucocorticoid signaling over UC to enhance biological interpretability. miR-mRNA interactions were prioritized based on database support and relevance to glucocorticoid receptor and inflammatory signaling as defined in the molecular mathematical model. Key transcriptional co-regulators within this network, including NCOA3, CBP, NCOR1, and NRIP1, distinguished response groups, together with miRs such as miR-145-5p, miR-10b-5p, and miR-16-5p. Several miR candidates showed circulating-tissue consistency and conserved behavior in a TNBS-induced colitis mouse model, in terms of expression in response to corticoids and miR-mRNA inverse correlations. This study proposes a mechanistically grounded framework for corticosteroid response biomarker discovery; however, findings are exploratory and prospective validation in independent cohorts is required before clinical applicability can be established. - Source: PubMed
Publication date: 2026/08/03
Ginés IrisSuau RogerNaves Juan EnriqueBernal CarlaClua LauraLorén VioletaPluvinet RaquelMonfort-Ferré DiandraLópez Balastegui MartaSánchez Herrero José FranciscoSegú-Vergés CristinaAransay Ana MariaBuschbeck MarcusMañosa MíriamSumoy LauroSerena CarolinaDomènech EugeniManyé Josep - Nuclear receptor coactivator 3 (NCOA3) is associated with various cancers, but its function and mechanism in glioblastoma multiforme (GBM) are still unclear. Bioinformatics analysis, in vitro cell experiments (NCOA3 silencing (si-NCOA3) or NCOA3 small-molecule inhibitor SI-2), in vivo animal models, and metabolic level detection were used to elucidate the activity of NCOA3 in GBM. The data revealed that GBM tissues had NCOA3 overexpression, which was linked with poor prognosis. It regulates pathways related to glycolysis, the cell cycle, and immunosuppression. Functionally, si-NCOA3/SI-2 suppressed GBM cell proliferation and migration. In vivo, sh-NCOA3/SI-2 demonstrated anti-glioma effects. Metabolically, treatment with si-NCOA3/SI-2 reduced glucose uptake, pyruvate and lactate production, ATP levels, and glycolysis-related enzyme expression in GBM cells. Combination therapy with SI-2 and TMZ enhanced GBM cell sensitivity to TMZ. Single-cell RNA sequencing revealed high NCOA3 expression in glioma stem cells (GSCs). si-NCOA3 inhibited GSCs proliferation and self-renewal while reducing the expression of Nestin and SOX2. NCOA3 is an oncogene in GBM. In mechanism, NCOA3 promotes GBM progression by enhancing the Warburg effect. In addition, NCOA3 is also highly expressed in GSCs and significantly promotes their proliferation and self-renewal ability. NCOA3 may represent a promising therapeutic target for GBM. - Source: PubMed
Publication date: 2026/08/13
Luo QianYang JiayingYin HailinYang MeiLiang YueyangHou YixuanSun XinzeLiu JixuanZhang Ling