IAP4 _ BIRC5
- Known as:
- IAP4 _ BIRC5
- Catalog number:
- NBP1-32035
- Product Quantity:
- 0.1 mg
- 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
- Mitochondrial outer membrane permeabilization (MOMP) is a core apoptotic regulatory event that dictates mitochondrial integrity, where full activation drives cell death and sublethal dysregulation contributes to tumor genomic instability. We used the Cancer Genome Atlas lung adenocarcinoma cohort (TCGA-LUAD) as the training cohort and the Gene Expression Omnibus dataset GSE42127 as the validation cohort to identify prognostic genes related to MOMP activity in lung adenocarcinoma (LUAD) and to evaluate their potential biological significance. By intersecting MOMP-related genes with differentially expressed genes, combined with survival analysis, Mendelian randomization analysis, and 101 machine-learning algorithm combinations, seven prognostic genes, namely BIRC5, PSMD11, TNFRSF13C, YWHAZ, YWHAG, CYCS, and LTB, were identified. Next, an optimal prognostic model was constructed based on the gradient boosting machine (GBM) algorithm. Based on the risk score, LUAD patients were stratified into high- and low-risk groups, and patients in the high-risk group exhibited poorer overall survival in both the training and validation cohorts. Furthermore, a nomogram integrating the risk score and clinicopathological factors was developed and showed favorable predictive performance for 1-, 3-, and 5-year survival. Meanwhile, functional and immune analyses revealed that the high-risk group was enriched in DNA replication-related pathways and demonstrated a higher tumor mutation burden (TMB). Correlation analysis indicated that TNFRSF13C was positively correlated with activated B cells, whereas BIRC5 was negatively correlated with eosinophils, suggesting that MOMP-related genes might be involved in remodeling the immune microenvironment of LUAD. Drug sensitivity analysis showed differences in predicted half-maximal inhibitory concentration (IC50) values between the risk groups, suggesting the potential value of this model in assisting therapeutic stratification. Single-cell RNA sequencing (scRNA-seq) further identified T lymphocytes as a key cell type, with numerous prognostic genes exhibiting differential expression in T cells or dynamic changes during differentiation. We suggest that the MOMP-related signature established in this study may provide a reference for prognostic stratification in LUAD and offers candidate prognostic genes for subsequent experimental and clinical validation. - Source: PubMed
Publication date: 2026/09/14
Liu DongmeiHe BinchanZhou XuanYang YuemeiSong MengyueXu Xiaoyong - Oral squamous cell carcinoma (OSCC) remains a clinically challenging malignancy because of recurrence, treatment resistance, and limited therapeutic efficacy in advanced disease. This study investigated the anticancer effects and molecular mechanisms of jaceidin (JAC), a naturally occurring flavonoid derivative, in human OSCC cells. SCC-1 and SCC-47 cells were treated with JAC, and cell viability, colony formation, cell cycle distribution, apoptosis, and apoptosis-related signaling pathways were examined. JAC reduced OSCC cell viability and colony formation in a dose- and time-dependent manner. It also induced G2/M cell cycle accumulation and decreased the expression of cyclin D1, cyclin E1, phosphorylated cdc2, and CDK2/4/6. Apoptosis analyses showed that JAC promoted caspase-dependent apoptotic signaling, as evidenced by increased cleavage of caspase-3, caspase-8, caspase-9, and PARP. JAC modulated death receptor-associated signaling, characterized by increased Fas, TRADD, and DR5 expression and caspase-8 cleavage, while the decoy receptors DcR2 and DcR3 were also upregulated. JAC also promoted mitochondrial apoptotic signaling by increasing Bax, Bak, and Bim expression while decreasing Mcl-1. In addition, JAC attenuated AKT and ERK1/2 phosphorylation, and pharmacological inhibition with LY294002 or U0126 further enhanced JAC-induced apoptotic signaling. Furthermore, JAC reduced survivin expression and attenuated survivin-mediated apoptotic resistance. These findings suggest that JAC suppresses OSCC cell survival in association with modulation of AKT/ERK-survivin signaling and caspase-dependent apoptosis. - Source: PubMed
Publication date: 2026/09/03
Hsieh Ming-JuHo Hsin-YuLin Chia-ChiehKao Min-YunLo Yu-ShengChuang Yi-ChingVelmurugan Bharath KumarChen Mu-Kuan - Liposarcoma (LPS) is a common soft tissue sarcoma; however, its molecular pathogenesis and immune cell infiltration remain poorly understood. This study investigated potential driver genes and pathways in LPS and characterized immune cell infiltration patterns to identify potential markers for targeted therapy. Differentially expressed genes (DEGs) in LPS were analyzed by GO and KEGG pathway enrichment analysis. A protein-protein interaction network was constructed using the STRING database and visualized with Cytoscape. mRNA expression of genes with high |logFC| values was verified by RT-qPCR. Immune cell subsets were quantified using CIBERSORT. GO and KEGG analysis revealed significant functional clusters and pathways, and most verified genes were consistent with the bioinformatics analysis. Survival analysis showed that high expression of TYMS, KIF20A, BUB1B, LMNB1, RRM2, ZWINT, and RACGAP1 was significantly associated with poor overall survival and poor disease-free survival (DFS). High levels of TMSB15A, TPX2, PKM2, and PTTG1 were significantly associated with poor DFS alone. CIBERSORT analysis identified a significantly higher fraction of resting mast cells (MCs) in LPS tissues compared to normal fatty tissues (P < 0.05). TOP2A, IL-6, PCNA, CDK1, JUN, MYC, CCNB1, EGFR, ACACB, and BIRC5 were identified as potential diagnostic biomarkers of LPS, providing strong evidence for hub gene studies. Immune cell infiltration analysis further suggested that resting MCs may play a potential role in LPS development, although further experimental validation is warranted. Collectively, these findings clarify the molecular basis of LPS and provide a foundation for future research into its treatment. - Source: PubMed
Publication date: 2026/09/11
Liu ChunxiaoWang YanhuaLiu QiuxiaZhang Sha - Breast cancer remains the most common cancer among women, with 2.3 million new cases reported globally in 2022. Alongside established risk factors such as age, family history, genetics, obesity, smoking, and alcohol, exposure to fine particulate matter (PM) has recently emerged as an environmental contributor. This risk is especially concerning for low- and middle-income countries (LMICs), where both PM exposure and cancer burden are disproportionately high; however, mechanistic studies from these regions remain limited. To address this gap and develop mitigation strategies, we investigated the oncogenic potential of water-soluble PM collected from ambient air on breast cancer and evaluated the potential role of nutraceuticals in mitigating these effects. PM exposure increased proliferation, migration, and ROS generation, while promoting the formation of multinucleated giant cells, leading to genomic instability. Berberine, a natural alkaloid, countered these effects by increasing DNA damage and exploiting tumor-specific genomic vulnerabilities through disruption of DNA damage response and repair networks, thereby promoting programmed cell death. Transcriptomic profiling of Delhi PM-treated MCF7 cells revealed a Delhi PM-associated carcinogenic gene signature enriched in MAPK signalling, reactive oxygen species, metabolic, lysosomal, and ribosomal pathways. We also found that several genes, including BIRC5, WSB1, and RCC1, within this PM-induced gene signature were dysregulated in breast cancer patients and were inversely regulated by berberine treatment, suggesting that berberine counteracts the transcriptional effects of PM. Our findings highlight ambient PM exposure as a driver of breast cancer progression and identify berberine as a promising candidate in mitigating PM effects; however, thorough preclinical and clinical validations are warranted. - Source: PubMed
Publication date: 2026/09/11
Bisht AnadiJaiswal AishwaryaSingh Rana PDey SagnikKulshreshtha Ritu - The tumor microenvironment (TME) is a complex ecosystem in which intercellular communication regulates tumor progression and therapeutic response. Yet inferring cell-cell interactions from non-spatial scRNA-seq remains challenging due to incomplete ligand-receptor databases and inaccurate cell type annotations. Here, we propose scGraphTrans, a graph neural network framework that integrates functional state pseudo-labels, graph structure learning, and graph domain adaptation to improve both cell type annotation and communication inference. Pathway activity scores across 14 cancer-relevant processes (e.g., angiogenesis, apoptosis, cell cycle) are used as pseudo-labels to refine cell-cell graphs, capturing functional proximity beyond geometric similarity. A domain adaptation module further aligns embeddings across patients, enhancing cross-individual generalization. Evaluated on 38,667 cells from 15 individuals across three cancers, scGraphTrans achieved an average accuracy of 84.28%, surpassing state-of-the-art baselines while maintaining robustness across heterogeneous datasets. Statistical validation demonstrated recovery of disease-specific gene interactions (e.g., LGALS1-SUSD2 in breast invasive carcinoma and BIRC5-CASP6 in colorectal cancer) without prior ligand-receptor supervision. The source code and data used in this paper can be found in https://github.com/LiYuechao1998/scGraphTrans. Our framework thus provides an interpretable and generalizable solution for TME analysis, offering insights into biomarker discovery and therapeutic strategies. - Source: PubMed
Publication date: 2026/09/10
Li Yue-ChaoYou Hai-RuWei Meng-MengWang Xin-FeiLi YuHuang Zhi-AnHuang Yu-AnYou Zhu-Hong