IAP4 _ BIRC5
- Known as:
- IAP4 _ BIRC5
- Catalog number:
- NB110-92717G
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- IAP4 _ BIRC5
Related genes to: IAP4 _ BIRC5
- Gene:
- BIRC5 NIH gene
- Name:
- baculoviral IAP repeat containing 5
- Previous symbol:
- API4
- Synonyms:
- EPR-1, survivin
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-04
Related products to: IAP4 _ BIRC5
Related articles to: IAP4 _ BIRC5
- Neuroblastoma (NB) exhibits profound clinical and molecular heterogeneity, highlighting the need for reproducible biomarkers for disease stratification. This study aimed to identify robust stage-associated gene signatures through integrative machine learning (ML) and cross-platform validation. Four independent NB microarray datasets were integrated to perform a multi-cohort meta-analysis. Differentially expressed genes (DEGs) were identified using Linear Models for Microarray Data (limma), followed by feature selection through three orthogonal ML models - Random Forest (RF), eXtreme Gradient Boosting (XGBoost), and Neural Network (NN). Overlapping markers among methods were used to define a consensus gene set, which was then compared with gene expression data from the Therapeutically Applicable Research to Generate Effective Treatments - Neuroblastoma (TARGET-NBL) cohort for clinical relevance assessment. We identified a seven-gene consensus set (BIRC5, CCDC127, AW473883, BRD7, TCF7L2, GABARAPL1, and CD1E) through ML, within which TCF7L2 emerged as a critical intersection between statistical and ML frameworks. While the large-scale 632-DEG set provided the broadest prognostic coverage, the refined seven-gene signature maintained robust clinical relevance. Notably, three mapped core genes (CD1E, GABARAPL1, and TCF7L2) were independently validated as significant favorable survival-associated markers (p < 0.05) in the TARGET cohort, even after rigorous clinical adjustment for age and COG risk status. By bridging transcriptomic discovery with cross-platform validation, this study establishes a high-confidence consensus gene signature for NB. Our findings suggest that while high-dimensional signatures offer extensive predictive power, the consensus-based core genes - particularly TCF7L2 - represent reproducible candidate biomarkers associated with disease progression and patient outcome. - Source: PubMed
Publication date: 2026/09/19
Liu DanielKuo JimmyWu Yao-ChongHsieh Shang-YuHuang An RongLin Chorng-Horng - Breast cancer exhibits substantial molecular heterogeneity, resulting in diverse therapeutic vulnerabilities and limiting the efficacy of single-agent therapies. Although multi-target strategies may offer improved therapeutic benefit, the systematic identification of synergistic higher-order target combinations remains challenging. This study aimed to identify and validate effective higher-order target combinations for heterogeneous breast cancer. DeepMDS, a previously developed deep learning-based multi-compound synergy prediction model, was used to prioritize candidate target combinations for breast cancer. Exhaustive two-target and three-target combinations were ranked in the gene-expression contexts of ER-positive luminal-like MCF-7 and triple-negative MDA-MB-231 breast cancer cells. The top-ranked target combinations were evaluated using single, pairwise, and triple small interfering RNA (siRNA) perturbations. Representative inhibitors were subsequently assessed in fixed-ratio combinations in MCF-7, MDA-MB-231, and 4T1 cells and in a 4T1 syngeneic mouse experiment. BIRC5-NAMPT-TOP1 ranked first in both cell lines. Triple siRNA co-transfection targeting , , and produced the strongest antiproliferative effects, with inhibition rates of 62.94% in MCF-7 cells and 55.62% in MDA-MB-231 cells. The corresponding inhibitors, LQZ-7I, FK866, and topotecan, exhibited synergistic antiproliferative activity at multiple molar ratios, with combination index values below 1. The optimized 2.5:10:1 molar ratio showed strong synergy in MCF-7, MDA-MB-231, and 4T1 cells, with combination index values of 0.26, 0.19, and 0.15, respectively. In tumor-bearing mice model, the triple-inhibitor regimen achieved a tumor inhibition rate of 62.05%. Topotecan-containing groups showed hematological alterations, whereas no statistically detectable elevations were observed in the measured terminal serum hepatic or renal biomarkers. The BIRC5-NAMPT-TOP1 combination showed reproducible phenotypic activity in the tested genetic and pharmacological models. These findings support the use of DeepMDS as a hypothesis-generation tool for higher-order target prioritization. - Source: PubMed
Publication date: 2026/08/28
Feng ChunlaiFeng QiuqiShe ShengnanYang RuojingLi MengruGong LuRui Mengjie - Drug repurposing represents an accelerated and cost-effective approach to discovering novel oncologic therapeutics. Here, we investigated the anticancer potential and underlying mechanisms of marbofloxacin (MBF), a veterinary fluoroquinolone (FQ), against breast cancer (BC) cells. The cellular impacts of MBF on cell viability, anchorage-dependent growth, tumorigenicity, migration, apoptosis, proliferation, senescence, and mitochondrial function were thoroughly characterized. To further elucidate its mechanistic activity, real-time qRT-PCR, untargeted LC-MS/MS-based metabolomics, network pharmacology, and molecular docking analysis were integrated. MBF suppressed BC cell growth by inhibiting cellular proliferation and migration, disrupting mitochondrial membrane potential, and inducing ROS-mediated apoptosis and irreversible cellular senescence. These phenotypic impacts were accompanied by upregulation of tumor suppressors such as and and downregulation of oncogenes including , , and . Metabolomic analysis revealed broad suppression of biosynthesis-related metabolic pathways, characterized by the depletion of critical polyamines and nucleotide pathways. Network pharmacology and molecular docking analyses identified EGFR and HSP90AA1 as putative hub proteins potentially associated with the observed anticancer phenotype. These results provide initial evidence that MBF induces metabolic and molecular rewiring in BC, highlighting its promise as a repositionable therapeutic candidate. - Source: PubMed
Publication date: 2026/08/22
Yavuz MervenurDewi Firli R PKeskin İlknurDemircan Turan - Cervical cancer represents a global public health problem, hence the importance of optimizing therapeutic options and expanding knowledge of prognostic markers. Clinical and experimental evidence shows that hypoxia-inducible factor (HIF) is a key inducer of aggressive phenotypes in cervical cancer: promoting angiogenesis, invasion, epithelial-mesenchymal transition (EMT), modulation of the immune microenvironment, and contributing to resistance to radiotherapy/chemotherapy in a possible synergistic effect with the human papilloma virus oncogenes. Hypoxic microenvironments that modulate the early activation of HIF pathways may be present in pre-invasive lesions and favor the acquisition of invasive phenotypes that precede invasion. This review highlights the mechanisms of HIF-1α in the progression of cervical intraepithelial neoplasia and cervical cancer. In this regard, HIF-1α is involved in the expression of genes related to angiogenesis, apoptosis and progression such as GLUT1, uPAR, BIRC5, EPO, EpoR, LIMD1, VHL, MET and pro-angiogenic genes (VEGF, PGF, PDGF-β, PAI-1, MMP-2, MMP-9, ANG-1, ANG-2, using pathways such as YAP/TA2. However, the balance between antitumor factors (miR-143) and protumor factors can define the progression of this neoplasia. In the future, the characterization of hypoxia signatures and the evaluation of HIF-1α pathway inhibitors are promising tools for optimizing outcomes in the treatment of cervical cancer, integrated with modern, high-precision radiation therapy techniques and predictive models based on imaging and artificial intelligence, which represent a key pillar of personalized oncology in cervical cancer, with the potential to improve tumor control and reduce toxicity; however, specific clinical trials are still needed to validate their impact on survival and safety. - Source: PubMed
Publication date: 2026/09/10
Carrero Yenddy NMosquera Jesús A - The main causes of posterior capsular opacification (PCO) are the proliferation, migration, and epithelial-mesenchymal transition (EMT) of leftover lens epithelial cells (LECs), though the exact mechanisms of EMT in PCO are not completely known. This research sought to determine whether PCO progression depends on Yes-associated protein 1 (YAP1) activation and EMT in LECs. We conducted gain- and loss-of-function experiments in human lens epithelial cells (HLE-B3) using YAP1-overexpressing plasmids and siRNA-YAP1. Cell migration was tested with a scratch wound assay, and Hippo/YAP signaling and EMT markers were analyzed via qPCR, Western blot, and immunocytochemistry. HLE-B3 cells were exposed to transforming growth factor-beta 2 (TGF-β2) and the YAP1 inhibitor verteporfin (VP) to evaluate cell proliferation, migration, and molecular expression using CCK-8, scratch assay, qPCR, and Western blot. A rabbit model for PCO was developed to test VP's effectiveness, evaluated by slit-lamp photography, H&E staining, immunofluorescence, and Western blotting for YAP1 and EMT-related proteins. In vitro, YAP1 overexpression increased TEAD2 and BIRC5, promoting EMT, while YAP1 knockdown reduced these proteins, inhibiting EMT. VP treatment decreased HLE-B3 proliferation and migration. Inhibiting YAP1 and its downstream targets, CTGF and BIRC5, suppressed EMT. In vivo, VP significantly delayed PCO progression in rabbits and decreased YAP1, α-SMA, and vimentin expression. These results suggest that YAP1 facilitates EMT in lens epithelial cells through the Hippo/YAP pathway, and its inhibition could be a promising strategy for PCO treatment. - Source: PubMed
Publication date: 2026/09/18
Su XingyuLiao JuanyuanJiang JiaojiaoLi JinqingHuang JianhuanZheng LiuDing Zhixiang