Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
- Known as:
- Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
- Catalog number:
- sr10030va-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Human Nanog Differentiation Reporter (pGreenZeo pre-packaged)
Related genes to: Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
- Gene:
- NANOG NIH gene
- Name:
- Nanog homeobox
- Previous symbol:
- -
- Synonyms:
- FLJ12581, FLJ40451
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-10
- Date modifiied:
- 2014-11-19
Related products to: Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
Related articles to: Human Nanog Differentiation Reporter (pGreenZeo, pre-packaged)
- Seminoma, which is the most frequent testicular germ cell tumor, has stem cell-like features related to treatment resistance and recurrence, yet the molecular mechanisms that preserve its stemness are not well understood. This study aimed to discover the tumorigenesis and stemness regulation of seminoma. In vivo CRISPR/Cas9 knockout library screening was performed using Tcam-2 seminoma cells implanted into NSG mice to identify tumorigenesis drivers. Parallel FACS-based screening enriched CD117/CD133 double-negative cells to assess the regulators of seminoma stemness. Functional validation included clonogenicity assays, sphere formation tests, and tumor initiation experiments in vivo. RNA sequencing analyzed downstream pathways. In vivo and FACS-based CRISPR/Cas9 screening uncovers VENTX as a crucial element in maintaining seminoma stemness. Functional validation showed that VENTX knockout decreased clonogenicity, sphere formation, and CD117+/CD133+ populations in Tcam-2 cells, and also hindered tumor initiation in vivo. RNA sequencing identified a connection between VENTX and pluripotency pathways, demonstrating a downregulation of ID1/2/3 (essential differentiation inhibitors) and an imbalance in Wnt/β-catenin and TGF-β signaling. VENTX expression showed a significant association with DNA methylation-based stemness scores in testicular germ cell tumors. In conclusion, VENTX is a key regulator of seminoma stemness, presenting a promising target for therapy to address recurrence and resistance in seminoma. - Source: PubMed
Publication date: 2026/09/03
Huang ChaoxiongChen YiranZhang EnhuanWang YifanLiu YixuanTang LiruiChen ChuanbenLin PeichengWang Bingyi - Lung cancer remains the leading cause of cancer-related mortality worldwide, largely due to therapeutic resistance and tumor recurrence. In non-small cell lung cancer (NSCLC), cancer stem cells (CSCs) have emerged as key contributors to tumor persistence and progression. However, accelerated CSC-targeted drug discovery is limited by the lack of scalable and quantitative screening systems capable of capturing stemness-associated phenotypes. Conventional two-dimensional (2D) assays often fail to reflect the architectural and molecular complexity of CSC-enriched tumor populations. Here, we report the establishment of a luciferase-based three-dimensional (3D) NSCLC spheroid platform integrating CSC-like enrichment with a high-throughput quantitative readout. The luminescent signal strongly correlated with spheroid burden and viable cell content. Compared with 2D monolayers, 3D NSCLC spheroids exhibited elevated expression of pluripotency-associated factors, including OCT4, NANOG, and SOX2, and CSC-associated markers, namely CD44, ALDH1A1, and ABCG2, supporting the enrichment of CSC-like subpopulations. As a proof-of-concept, screening of renieramycin T right-half derivatives identified DH_18 as a lead compound in the established 3D NSCLC spheroid model, exhibiting greater potency than DH_19, accompanied by increased apoptosis and reduced CSC-associated proteins in follow-up experimental validation. Integrated network pharmacology incorporating enrichment and protein-protein interaction analyses further mapped DH_18-NSCLC targets to lung CSC-associated networks and pathways related to stemness and aggressive tumor phenotypes, reinforcing the biological relevance of the 3D screening context. Collectively, these findings present a quantitative and scalable 3D NSCLC spheroid platform suitable for CSC-targeted drug screening and nominate DH_18 as a candidate compound with potential activity against stemness-linked molecular networks. - Source: PubMed
Publication date: 2026/09/01
Samart ParinyaChanthateyanonth SupasornRodboon NapachaiCharoenvitayavorakul NititYamada TatsukiYokoya MasashiChanvorachote PithiIssaragrisil SurapolLuanpitpong Sudjit - Colorectal cancer (CRC) remains a major cause of cancer-related mortality due to therapeutic resistance. Because colorectal cancer stem-like cells (CRCSCs) play a central role in tumor initiation and progression, therapeutic strategies addressing CSC-enriched populations are urgently needed. In this study, we investigated the anticancer effects of emodin, a natural anthraquinone, in CSC-enriched tumorsphere models. Emodin significantly suppressed the viability and self-renewal capacity of HCT116- and SW480-derived CSCs. It induced G0/G1 cell cycle arrest and markedly downregulated stemness-associated markers (CD44, CD133, ALDH1A1, SOX2, NANOG, and OCT4). Importantly, emodin-induced cell death was characterized by mitochondrial dysfunction, increased mitochondrial reactive oxygen species, loss of membrane potential, and nuclear translocation of apoptosis-inducing factor (AIF). This cytotoxicity was not rescued by the pan-caspase inhibitor Z-VAD-FMK, confirming caspase-independent apoptosis. Furthermore, network pharmacology and experimental validation identified GSK3β as a key target. Emodin reduced Wnt/β-catenin signaling by decreasing β-catenin stabilization and nuclear accumulation. Crucially, a rescue experiment utilizing LiCl confirmed that emodin's suppressive effects are mechanistically dependent on the GSK3β/Wnt/β-catenin axis. Collectively, emodin suppresses CRCSC characteristics by downregulating Wnt/β-catenin signaling and inducing AIF-associated caspase-independent apoptosis, highlighting its therapeutic potential against CRC. - Source: PubMed
Publication date: 2026/08/31
Ahmadi MahdiehKim Hong LaeJung Hye Jin - The low efficiency in the production of induced pluripotent stem cell (iPSC) remains a major barrier to the widespread reprogramming applications in regenerative medicine and drug screening. Small molecules that modulate key signaling pathways offer a promising approach to overcome the reprogramming limitation. Here, we demonstrated that Thiazovivin (TZV), a selective Rho-associated coiled-coil kinase inhibitor, significantly increased human fibroblast reprogramming rate by approximately 1.4-fold (* < 0.01). Treatment with TZV during the early phase of reprogramming enhanced colony formation, improved cell survival, and promoted the mesenchymal-to-epithelial transition (MET). Quantitative Real Time Polymerase Chain Reaction (RT-PCR) analysis revealed the downregulation of mesenchymal markers (N-cadherin, 52%; vimentin, 61%; < 0.05) and upregulation of epithelial markers (E-cadherin, 165%; EpCAM, 95%; < 0.05). Flow cytometry confirmed elevated expression of NANOG and TRA-1-60 pluripotency markers. Collectively, these findings suggest that TZV facilitates reprogramming through MET, offering a simple and effective strategy to enhance the efficiency and scalability of human iPSC generation. - Source: PubMed
Publication date: 2026/08/31
Azhdari MahsaDehghan SamanehGhamari AliMirshahi RezaShoae-Hassani Alireza - : This study engineered and evaluated a targeted, folate-functionalized chitosan nanoparticle (CS-FA NP) delivery system to enhance the therapeutic efficacy of standard quercetin and seed extract against breast cancer. : Phytochemical profiling confirmed a 14% crude yield for the methanolic extract, with gas chromatography-mass spectrometry (GC-MS) and high-performance liquid chromatography (HPLC) identifying quercetin as the principal bioactive agent. The synthesized CS-FA NPs exhibited a core size of 7-20 nm, an average hydrodynamic diameter of 150-160 nm, a stable zeta potential of -55 mV, and high encapsulation efficiencies (87.2% for quercetin and 80.5% for coriander). Kinetic assessments confirmed a biphasic, diffusion-controlled release matching Higuchi matrix kinetics. Anticancer activity was evaluated in vitro using MTT cytotoxicity, Annexin V-FITC/PI apoptosis analysis, RT-qPCR, and ex vivo rat aortic ring assays, followed by validation in a syngeneic 4T1 mammary tumor mouse model. : In vitro, folate-receptor-targeted quercetin nanoparticles (T4) demonstrated superior, selective cytotoxicity, particularly against triple-negative MDA-MB-231 cells, while sparing normal fibroblasts. Annexin V-FITC/PI apoptosis profiling and ex vivo aortic ring assays revealed profound, cell-line-dependent programmed cell death and up to 90% inhibition of microvessel sprout outgrowth. Mechanistically, RT-qPCR verified that nano-formulations induced complete transcriptional silencing of NANOG, MMP-1, VEGFA, TSPAN8, TWIST, EMMPRIN, and CDK1, alongside marked upregulation of P27 and P21. In vivo, these nano-formulations successfully improved tumor-associated pathological features, reduced aggressive tumor spindle-cell proliferation, and suppressed elevated serum CA15-3 and arginase biomarkers. : Folate-functionalized chitosan nano-formulations significantly enhanced the anticancer efficacy of quercetin and seed extract through improved targeted delivery, potent antiproliferative, anti-angiogenic, and pro-apoptotic activities, together with favorable modulation of multiple molecular pathways associated with breast cancer progression. These findings support their potential as promising targeted nanotherapeutic strategies for breast cancer treatment. - Source: PubMed
Publication date: 2026/08/12
Nabil NarimanSabit HusseinAlmulhim JawaherArneth BorrosAbdel-Ghany Shaimaa