IAP4 _ BIRC5 (C_term)
- Known as:
- IAP4 _ BIRC5 (C_term)
- Catalog number:
- AP16261PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- IAP4 _ BIRC5 (C_term)
Related genes to: IAP4 _ BIRC5 (C_term)
- 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 (C_term)
Related articles to: IAP4 _ BIRC5 (C_term)
- : Recurrence poses a major challenge in epithelial ovarian cancer (EOC), often occurring despite optimal first-line therapy. Dormant cancer cells are believed to play a key role, yet the mechanisms driving their reactivation remain unclear. This study examined whether exosomes released by normal peritoneal mesothelial cells (PMCs) and fibroblasts (PFBs) undergoing iatrogenic senescence after carboplatin and paclitaxel exposure contribute to EOC recurrence. : Senescent PMCs and PFBs secreted markedly more exosomes, identified by CD9, CD63, and CD81, compared with young cells. Exosomes from both cell types more effectively reactivated dormant EOC cells (pEOCs, A2780, OVCAR-3, SKOV-3) than non-exosomal medium constituents. Importantly, senescent PMC-derived exosomes most strongly reactivated pEOCs and SKOV-3, whereas those from senescent PFBs exerted greater effects on pEOCs, OVCAR-3, and SKOV-3. Kinetic studies of exosome internalization revealed that this process was generally more efficient in the presence of exosomes derived from senescent cells compared with those from young donor cells. Compositional analysis revealed distinct profiles between young and senescent exosomes compared in two variants: young PMCs/senescent PMCs and young PFBs/senescent PFBS. Senescent PMC exosomes displayed reduced miR-210-3p, miR-409-3p, and miR-421, alongside elevated MMP1, MMP3, and VEGF, while senescent PFB exosomes showed increased amphiregulin and osteopontin but lower MMP1, MMP3, TIMP1, bFGF, VEGF, and HGF. Functionally, senescent PMC exosomes enhanced pEOC migration, invasion, and spheroid formation, and induced the expression of CCL11 and ABCB1. Senescent PFB exosomes promoted migration and upregulated CCL11, TGF-β1, BIRC5, and CHEK1. : These findings suggest that therapy-induced senescence in peritoneal cells may contribute to EOC recurrence by reactivating dormant tumor cells through exosomal signaling. - Source: PubMed
Publication date: 2026/04/23
Rutecki SzymonKrawiec AdriannaLeśniewska-Bocianowska AgnieszkaMatuszewska JuliaNaumowicz ErykSzubert SebastianKsiążek KrzysztofMikuła-Pietrasik Justyna - Deltamethrin (DM) is a common type II synthetic pyrethroid pesticide; however, increasing evidence indicates that long-term exposure can cause systemic toxicity. This toxicity is linked to inflammation due to oxidative stress and cell death, possibly involving microRNA disruption of antioxidant defenses. This study aimed to explore how a combination of chitosan and ivy leaf extract (Hedera helix) protects against liver, kidney, and reproductive toxicity caused by DM exposure. It specifically examines the role of miR-144 in antioxidant pathways. Forty-eight adult male Wistar rats were divided into eight groups. They received oral treatments for 90 days, including DM (0.6 mg/kg), chitosan (200 mg/kg), ivy leaf extract (50 mg/kg), or combinations of these. Liver and kidney functions, markers of oxidative stress (MDA, GPx, SOD), inflammatory markers (TNF-α, COX-2, MAPK14), apoptotic markers (Bax, Caspase-3, Birc5), and the expression of miR-144 were assessed, along with comprehensive histopathological and immunohistochemical evaluations. Subchronic DM exposure led to significant weight loss and multi-organ dysfunction. This was associated with a marked increase in lipid peroxidation and a decline in antioxidant defenses. Molecular analysis revealed that DM significantly increased miR-144 expression in the liver, kidney, and testis, with a strong negative correlation with SOD activity (r - 0.916 in the kidney and -0.911 in the liver). This redox imbalance was associated with an inflammatory response via MAPK14 and shifted the balance toward apoptosis. Notably, the combination of chitosan and ivy leaf extract provided greater protection than either treatment alone, with lowered miR-144 levels, restored antioxidant enzyme activity, and reduced pro-inflammatory and apoptotic signals, and a clear restoration of tissue structure toward normal. The findings suggest a superior combined protective effect. Chitosan acts by scavenging free radicals, while ivy leaf extract likely involves modulation of the miR-144-associated antioxidant pathway. This highlights the potential of using natural antioxidant combinations to counteract the long-term effects of pesticide toxicity. - Source: PubMed
Publication date: 2026/05/12
Moawad Asmaa MohammadShaban FatmaAttia Abla AbdelmeguidAbdelgwad MarwaHosny Sara AdelAbouelkeir Abrar RoshdyElkady Nevine Khairy - Bisphenol A (BPA), an environmental endocrine disruptor, is implicated in hepatocellular carcinoma (HCC), but its molecular mechanisms are unclear. This study employed an integrative computational framework to identify potential BPA-related molecular targets in HCC, assess their statistical clinical value, and generate hypotheses regarding their roles within the tumor microenvironment. BPA and HCC targets were retrieved from public databases and intersected with differentially expressed genes in HCC, identifying fifteen overlapping genes statistically enriched in cell cycle regulation, p53 signaling, and viral carcinogenesis. Six hub genes (MKI67, CCNA2, EZH2, CCNB1, CDK1, BIRC5) were significantly upregulated in HCC with high internal cross-validated diagnostic accuracy (AUC > 0.96), although these estimates may be susceptible to overfitting and require external validation. Molecular docking and dynamics simulations predicted stable BPA binding to six proteins (Ki67, Cyclin A2, EZH2, Cyclin B1, CDK1, Survivin), with van der Waals forces calculated as the primary driving energy contribution by MM-PBSA. The two-gene (CCNB1/EZH2) risk model showed statistical associations with patient survival, validated internally and externally, although its generalizability remains limited. Mendelian randomization provided genetic evidence consistent with a potential risk-associated role for CCNB1 and a protective-associated role for EZH2. Single-cell analysis localized high CCNB1 and EZH2 expression to malignant and proliferative T-cells, correlating with specific immune infiltration patterns and checkpoint expression. In conclusion, these computational findings suggest a statistical and structural association between BPA exposure and HCC-related core cell-cycle regulators (e.g., CCNB1/EZH2). The data generate the hypothesis that CCNB1 and EZH2 may serve as prognostic biomarkers and potential contributors to HCC biology, possibly through coordinated effects on cell cycle dysregulation and immune microenvironment remodeling, though direct evidence of in vivo molecular targeting by BPA or causal pathway activation is not established by this study. These findings provide novel insights into BPA's putative role in hepatocarcinogenesis and offer clues for future experimental validation regarding risk assessment and therapeutic strategies. - Source: PubMed
Publication date: 2026/05/12
Zeng FulingLai FuyanZeng Jiaxin - Breast cancer remains a significant global health challenge, necessitating the development of innovative therapeutic strategies. This study aims to integrate immunotherapy and suicide gene therapy for breast cancer treatment. The cytokines IL-2 and GM-CSF, which are crucial in orchestrating immune responses against cancer, are the focal points of investigation. This study focused on the co-expression of these cytokines alongside apoptin, a promising protein derived from chicken anemia virus, via the bidirectional survivin promoter (pAIG). The constructed vectors were transfected into MCF-7 cells, which resulted in a significant increase in gene expression. Compared with individual cytokine and apoptin vectors (pIG and pA), the pAIG vector exhibited superior efficacy, reducing cell viability and inducing apoptosis (31.7%) at 72 h post-transfection. Exploration of the interaction of apoptin revealed its association with the human PIK3R1 protein, which interacts with both cytokines, contributing to the inhibition of cell viability. Leveraging the survivin promoter for co-expression presents a promising avenue for targeted breast cancer gene therapy, potentially disrupting intricate signaling networks involved in cancer progression. This study provides valuable insights into the synergistic effects of IL-2, GM-CSF, and apoptin co-expression, offering a compelling approach to advancing breast cancer treatment. These findings contribute to the broader landscape of cancer gene therapy, emphasizing the potential of combining immunomodulatory agents and gene-directed approaches to improve therapeutic outcomes. - Source: PubMed
Barzegari OmidGhadimi FatemehShamsabadi Fatemeh TGolalipour MasoudShahbazi Majid - Whole-genome doubling (WGD) is a common yet poorly understood event associated with poor clinical outcomes. Here, we characterize mechanisms by which WGD drives tumor evolution, utilizing mouse mammary tumor models of WGD established through cell fusion. We find that WGD increases transcriptomic and epigenetic heterogeneity and identify the YM155 BIRC5 inhibitor as a compound specifically suppressing WGD+ tumors. WGD triggers immune evasion by escaping CD8 T cell responses, rendering WGD+ tumors more sensitive to anti-PD-L1. Through single-cell profiling, we discover that WGD+ cancer cells exhibit reduced antigen presentation and response to IFNγ, attributed to the epigenetic silencing of MHCI transcriptional regulators via elevated histone H3 lysine 27 trimethylation. Further investigations reveal decreased KDM6 activity and increased succinate levels in WGD+ tumors. PRC2 inhibition preferentially suppresses WGD+ tumor growth, enhances antigen presentation, and CD8 T cell infiltration. Our results underscore metabolic and epigenetic alterations as critical drivers of WGD-associated immune escape. - Source: PubMed
Publication date: 2026/05/07
Foidart PierreLi ZheqiCai XinranSeehawer MarcoBrown Daniel DTawawalla AmatullahBaldominos PilarParvin SalmaNishida JunRojas-Jimenez ErnestoBui Triet MDiciaccio BenedettoKumar RahulSchlegel Brent TGoyette Marie-AnneScales TashJaeYan PengzeQiu XintaoLi RongJiang YijiaXie YingtianAarabi MahmoudHuang Xiao-YunStevens Laura ECejas PalomaMangiante LiseSotomayor Vivas Cristina IreneHoulahan Kathleen ECurtis ChristinaOesterreich SteffiHarris Isaac SLetai Anthony GLee Adrian VLong Henry WAgudo JudithPolyak Kornelia