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
- Unlike adult hearts, neonatal hearts can regenerate and adapt to stress. To identify both cardioprotective and regenerative mechanisms, we compared activated genes and related signaling pathways in the neonatal mouse heart after myocardial infarction (MI) and after exposure to pressure overload using a neonatal model of transverse aortic constriction (nTAC) at postnatal day 1 (P1). We identified three immune-related genes-Ccl4, S100a8, and C1qa-of high interest, as they encode secreted factors, are highly expressed in the neonatal mouse heart in both injury types, and their receptors are expressed on neonatal cardiomyocytes (nCM) and cardiac endothelial cells (EC). We investigated their effects on primary mouse EC and nCM in vitro. Our study found that the combination of these secreted factors (Pool3) enhances EC and nCM cell cycle re-entry and reduces the rate of apoptosis. Combined in vivo and in vitro transcriptome analyses revealed that Toll-like receptor 2 (TLR2) activation in nCM induces a shared pro-survival and cell cycle re-entry-associated signaling, including upregulation of Bcl2 and Birc5, respectively. The direct and pivotal role of TLR2 in enhancing nCM cell cycle re-entry and survival was further confirmed using TLR2 knockout (KO) nCM, a TLR2 inhibitor, and a TLR2 agonist (zymosan). Moreover, the importance of TLR2 in mediating the adaptive response to pressure overload in neonatal mice was confirmed in TLR2 KO mice, which failed to adapt to pressure overload and exhibited high mortality together with maladaptive cardiac remodeling as early as 7 days post-surgery. Collectively, these findings demonstrate that TLR2 is essential for mediating nCM cell cycle re-entry, survival, and adaptive/regenerative response to injury. - Source: PubMed
Publication date: 2026/08/14
Nicke JuliaGoldspink AdrianMenn MalteFleischmann Bernd KMalek Mohammadi Mona - Oral carcinoma is the sixth most prevalent cancer type with a poor 5-year survival rate. mRNA-lipid nanoparticle-based immunotherapy can overcome the challenges associated with conventional treatment options. Here, we investigated the immunogenicity and antitumor efficacy of survivin antigen encoded mRNA lipid nanoparticles (LNPs) in combination with anti-CTLA-4 immune checkpoint inhibitor. Survivin mRNA was synthesized by in vitro transcription technique after cloning the antigenic target sequence into an expression vector. The mRNA-LNPs were prepared with lipids, ALC-0315, DOPE, and cholesterol using a droplet-based microfluidic device. The average particle size, polydispersity index and encapsulation efficiency of mRNA-LNPs was found to be 305 ± 68 nm, 0.11, and 65 ± 3.9%, respectively. Survivin mRNA-LNPs incubated with mouse-derived bone marrow dendritic cells showed activation of tumor-associated antigen specific T-cells. The co-culture of splenocytes, and cheek cells derived from C57BL/6 mouse administered with survivin mRNA-LNPs and CTLA-4 inhibitor with MOC-1 oral carcinoma cells showed significant (P < 0.05) reduction in the cancer cell viability compared with control group. The oral cancer cytotoxicity is attributed to the upregulation of MHCI and MHCII, CD8 + and CD4 + T-lymphocytes and reduction in the T-regulatory cells. Taken together, this study provides preliminary evidence for further development of survivin mRNA-LNPs and CTLA-4 inhibitor combination for oral cancer immunotherapy. - Source: PubMed
Publication date: 2026/08/07
Krishna VandanaGoyal Srashti GopalVenuganti Venkata Vamsi Krishna - IntroductionFirst-generation EGFR-TKIs in NSCLC frequently lose efficacy as a result of the secondary EGFR-T790M mutation and a "persistent-STAT3" prosurvival pathway that sustains STAT3-survivin signaling in the face of EGFR inhibition. Preclinical evidence demonstrates that phytochemicals in the JI017 herbal formulation (2:1:1, : processed : ) can reinstate erlotinib sensitivity in T790M-positive NSCLC, and relevant molecular mechanisms have been examined.MethodsAnti-proliferative activities were evaluated in A549 (EGFR-WT), HCC827 (EGFR Δ19), and H1975 (EGFR L858R/T790M) cells utilizing MTT assays, colony formation, and Annexin V/7-AAD flow cytometry. Mechanistic analyses included immunoblotting for p-EGFR (Tyr1068/1173), p-JAK2, p-STAT3 (Tyr705), PARP, Bcl-2, survivin, and AXL, complemented by RT-qPCR for BIRC5 and AXL transcripts. Drug interaction effects were determined using the Chou-Talalay combination index (CompuSyn). Anti-tumor efficacy was assessed in H1975 xenografts treated for 14 days with vehicle, JI017, erlotinib, or combination therapy; tumors underwent H&E staining and IHC for p-STAT3, survivin, and Ki-67.ResultsJI017 inhibited proliferation in all NSCLC cell lines tested, showing greatest effectiveness in H1975, where it triggered PARP cleavage and suppression of Bcl-2 and survivin expression. In H1975, co-treatment with JI017 and erlotinib led to synergistic growth inhibition, eradicated colony growth, and significantly elevated apoptotic cell populations compared to single treatments. While erlotinib alone reduced p-EGFR and p-JAK2, it left p-STAT3 largely unaltered, reflecting persistent-STAT3 activity. The combination regimen abrogated p-STAT3, further lowered p-EGFR and p-JAK2 levels, diminished BIRC5 mRNA, and decreased both AXL protein and transcript levels. In vivo, the drug combination achieved sustained tumor stasis relative to controls or monotherapy; combination group tumors displayed widespread necrosis and substantial decreases in p-STAT3, survivin, and Ki-67.DiscussionThese data support the suppression of STAT3-survivin as the primary mechanism by which JI017 sensitizes EGFR-T790M models to erlotinib. The consistent down-regulation of AXL indicates the inhibition of an AXL-mediated bypass that may maintain STAT3 signaling during EGFR blockade, although causality has yet to be confirmed. The marked in-vivo tumor inhibition without observable toxicity underscores the translational promise as a low-toxicity therapeutic adjunct.ConclusionsJI017 restores erlotinib sensitivity in EGFR-T790M NSCLC by inhibiting STAT3-survivin signaling and possibly reducing AXL-mediated resistance, resulting in durable antitumor effects both in vitro and in vivo. Additional preclinical studies and early-phase clinical assessment of JI017 in combination with erlotinib are justified. - Source: PubMed
Publication date: 2026/08/04
Kim DaeunKim Young-HaChoi GaeunCheon ChunhooKo Seong-Gyu - Retinoblastoma (RB) lacks effective targeted therapies. Super-enhancers (SEs) are crucial for tumorigenesis, yet their role in RB was unclear. - Source: PubMed
Publication date: 2026/08/03
Guo CaiyaoDai WeiLi JingxuanZhou XuanYang JianqiongXie FenfenLiang WanZhou JingfengHou WenLan JinxiaLiu HaiLiu Shenglan - 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
Benchekroun SaraHammache MeriemChandad FatihaAlmutairi Mikhlid HDaich AdamBadwelan MohammedRouabhia MahmoudSemlali Abdelhabib