BIRC5 Over-expression Lysate
- Known as:
- BIRC5 Over-expression Lysate
- Catalog number:
- LY12234a
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- BIRC5 Over-expression Lysate
Related genes to: BIRC5 Over-expression Lysate
- 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: BIRC5 Over-expression Lysate
Related articles to: BIRC5 Over-expression Lysate
- 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 - Lip and oral cavity cancers are among the most common types of cancer worldwide and remain a major health problem due to poor prognosis and treatment- related side effects. Therefore, identifying new naturally derived compounds with selective cytotoxic effects on oral cancer cells is essential. Vulpinic acid, a lichenderived secondary metabolite, has shown antioxidant and anticancer activities in various cancer types. However, its effects on oral cancer cells have not yet been clarified. This study aims to investigate the cytotoxic and apoptotic effects of vulpinic acid on oral cancer cells and to explore its possible molecular mechanisms. - Source: PubMed
Publication date: 2026/05/04
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