c-IAP2 Monoclonal Antibody [16E63]
- Known as:
- c-IAP2 Monoclonal Antibody [16E63]
- Catalog number:
- A-0519-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- c-IAP2 Monoclonal Antibody [16E63]
Related genes to: c-IAP2 Monoclonal Antibody [16E63]
- Gene:
- BIRC3 NIH gene
- Name:
- baculoviral IAP repeat containing 3
- Previous symbol:
- API2
- Synonyms:
- cIAP2, hiap-1, MIHC, RNF49, MALT2, c-IAP2
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-05
Related products to: c-IAP2 Monoclonal Antibody [16E63]
Related articles to: c-IAP2 Monoclonal Antibody [16E63]
- L.f., a traditional medicinal plant widely distributed in South and Southeast Asia, has long been used in ethnomedicine to treat respiratory disorders, inflammation and tumor-related conditions. Although previous studies have suggested that possesses cytotoxic and anti-inflammatory activities, the antitumor efficacy and underlying mechanisms of its fruit-derived dichloromethane extract remain unclear. This study aimed to investigate the anti-lung cancer activity of the dichloromethane extract of fruits (FHF-DE) using integrated phytochemical, cellular, transcriptomic and approaches. FHF-DE inhibited the proliferation of multiple human lung cancer cell lines (including H1299, A549, H1975, H460, and PC9 cells) as well as murine Lewis lung carcinoma (LLC) line. Flow cytometry indicated G0/G1 arrest in LLC cells and S-phase arrest in H1975 cells. FHF-DE also promoted apoptotic cell death, as indicated by increased Bax expression, decreased Bcl-2 expression, and caspase-3 activation. Transcriptome sequencing and reverse transcription-quantitative (RT-q) PCR analyses indicated enrichment of the TNF signaling pathway, with increased TNF- and related gene expression (e.g., IRF1, BIRC3). In an LLC allograft mouse model, daily oral administration of FHF-DE (200-400 mg/kg) significantly suppressed tumor growth, without evident hepatotoxicity or nephrotoxicity in H&E staining. This finding demonstrates the antitumor efficacy of FHF-DE, although, molecular validation of the proposed mechanism in tumor tissues was not performed. Collectively, our in vitro data demonstrate that FHF-DE induces apoptosis and cell cycle arrest in lung cancer cells, with transcriptomic and pharmacological data suggesting a functional association with TNF-related signaling pathways. However, definitive mechanistic proof of direct TNFR1 engagement or extrinsic apoptotic pathway activation, particularly in vivo, requires further investigation. The present study provides preclinical evidence supporting further pharmacological and toxicological evaluation of fruit-derived extracts as natural-product-based candidates for lung cancer intervention. - Source: PubMed
Publication date: 2026/07/15
Yang JuanWu WenmingPeng JiahuiLiu XiaoyuYing DongmeiZhou XinyiWang JunanDuan YoufaXiong WenchaoJin An - Nasopharyngeal carcinoma (NPC) is a head and neck cancer characterized by highly locoregionally invasive behavior attributable to the latent infection with Epstein-Barr virus (EBV) and genomic instability. It is well established that EBV-encoded oncogenic molecules actively contribute to the malignant behavior of NPC cells. However, the mechanism by which aberrant genomic alterations enable NPC cells to become aggressive remains largely unknown. In the present study, whole-exome sequencing (WES) revealed that the gene encoding the baculoviral IAP repeat-containing 3 (BIRC3) protein was frequently mutated in circulating tumor cells (CTCs) but not in paired primary tumor cells from patients with metastatic NPC. A minigene assay indicated that the c.637 A > G mutation disrupted normal mRNA splicing, resulting in the partial deletion of Exons 2 and 3 and altered stability of BIRC3 mRNA. In vitro experiments demonstrated that ectopic expression of the BIRC3 mutant enhanced NPC cell invasive properties, including proliferation, resistance to apoptosis, migration, and invasion. Furthermore, overexpression of wild-type BIRC3 promoted invasive characteristics in NPC cells through the TRAF2-NF-κB signaling axis. In summary, BIRC3 acts as a regulator of the malignant features of NPC cells. Frequent BIRC3 mutations in CTCs, such as the c.637 A > G mutation, further enhance the metastatic potential of disseminated NPC cells by inducing aberrant alternative splicing. These findings suggest the therapeutic feasibility of targeting the BIRC3/TRAF2/NF-κB axis in the treatment of NPC. - Source: PubMed
Publication date: 2026/08/11
Liu XueLiu YupingZhu BiyunHuang YujuanChen YongLi QiuyunDeng YayanHuang LihongCai BinliFan QianqingLuo WenhuiYe JiaxiangLi YongqiangWei JiazhangZhang Jinyan - Primary cutaneous T-lymphomas (CTCL), particularly in their early stages, frequently present with clinical and histopathologic features that overlap with atopic dermatitis (AD) and psoriasis, contributing to diagnostic delay and ineffective, or even deleterious, treatment approaches. Thus, minimally invasive molecular tests capable of distinguishing CTCL from benign inflammatory dermatoses are urgently needed. - Source: PubMed
Publication date: 2026/08/07
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Publication date: 2026/07/17
Zhang HongliangCai Helun - This study aimed to investigate the selective anticancer activity of the curcumin analog PAC (3,5-Bis-4-hydroxy-3-methoxybenzylidene)-N-methyl-4-piperidone). Normal gingival epithelial cells (GECs), cancerous gingival cells (Ca9-22) and tongue squamous carcinoma cells (CAL27) were exposed to increasing concentrations of PAC (0-10 µM) for 24 h. Cell viability and cytotoxicity were evaluated using MTT and LDH assays, while apoptosis and caspase activation were analyzed by Annexin V/PI staining and flow cytometry. Gene-expression profiling was performed using RT Profiler PCR arrays. PAC significantly inhibited Ca9-22 and CAL27 cell proliferation in a concentration-dependent manner, with an IC value of 5 µM, while exerting no noticeable cytotoxic effects on normal GEC. PAC treatment induced significant early and late apoptosis associated with increased caspase activity in both oral cancer cell lines. Transcriptomic analyses revealed extensive modulation of apoptosis-related genes. In Ca9-22 cells, PAC predominantly suppressed anti-apoptotic and survival-associated genes, including BCL2, BIRC3, BIRC5, XIAP, CFLAR, and NFKB1. In contrast, CAL27 cells exhibited a more pronounced pro-apoptotic transcriptional profile characterized by upregulation of TP53, APAF1, CASP1, BID, and TNF. Gene interaction network analyses further demonstrated that PAC targets highly interconnected apoptotic signaling pathways. Collectively, these findings demonstrate that PAC exerts potent selective anticancer activity against OSCC cells through modulation of intrinsic and extrinsic apoptotic pathways. These results further support the therapeutic potential of PAC as a promising multitarget candidate for oral cancer treatment. - Source: PubMed
Publication date: 2026/06/23
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