Ask about this productRelated genes to: Nanog antibody
- 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: Nanog antibody
Related articles to: Nanog antibody
- The incidence and mortality of pancreatic cancer are steadily increasing worldwide, and the disease is projected to become the second leading cause of cancer-related deaths by 2030. Pancreatic tumorigenesis is driven by multiple genetic alterations, underscoring the need to elucidate the molecular mechanisms underlying pancreatic carcinogenesis. In this context, the present study is the first to identify a novel oncogenic role for Engrailed 2 (EN2) in the initiation and progression of pancreatic cancer and to characterise its underlying molecular pathogenesis. Immunohistochemical analysis of a pancreatic cancer tissue microarray revealed significantly elevated EN2 expression in tumour tissues compared with adjacent normal tissues. Consistent with these findings, EN2 was markedly upregulated in human pancreatic cancer cell lines, but absent in normal pancreatic epithelial cells, and functional studies demonstrated that EN2 expression is oncogenic in pancreatic cancer. TCGA data further corroborated the significantly higher EN2 expression in pancreatic cancer tissues and showed that elevated EN2 levels are associated with poor overall survival. To define the biological significance of EN2, we investigated its role in promoting pancreatic cancer initiation and progression. Gain- and loss-of-function studies revealed that EN2 regulates key target genes involved in pluripotency, cell survival, and cell-cycle progression, drug resistance, and epithelial-mesenchymal transition. Moreover, lentiviral-mediated shRNA knockdown of EN2 suppressed pancreatic cancer cell proliferation, invasion, and metastasis in vitro and significantly inhibited tumour growth in a xenograft mouse model, in part by inhibiting Notch signalling. Taken together, these findings identify EN2 as a critical driver of pancreatic cancer initiation, progression, and metastasis, representing the first report of its oncogenic function in this malignancy. - Source: PubMed
Yu WeiVarma Raj KMa YimingBoinpelly Varun ChandraKhatri AreejGombos EmmaSrivastava Rakesh KShankar Sharmila - Liver progenitor cells (LPC) exhibit the potential to differentiate into both hepatocytes and cholangiocytes, making them promising candidates for cell therapy in cases of severe liver pathology. However, the mechanisms of LPCs regeneration are unclear. Here, we utilised rat liver stem-like epithelial cells (WB-F344) in a wound-healing assay. The scratched near-confluent monolayer (70% area removed) underwent G1-arrest, transient bi-nucleation at 10-12 h post-injury, the epithelial-mesenchymal transition, and motion of cell fraction into the wounded areas. The transient displacement of the nuclear NANOG with upregulated p16, loss of epithelial albumin and CK7 markers, along with transient YAP1/Hippo and TWIST 1 activation, was seen near the wound edge. At 24 h, G1-arrest was overcome, followed by a proliferation boost. At 40-48 h, proliferation was accomplished by reconstitution of epithelial tissue, NANOG was restored in the cell nucleus, and p16 left it. Thus, wound healing was performed by concerted, molecular and cellular, bistable circuits. - Source: PubMed
Publication date: 2026/04/25
Lazovska MarijaSalmina KristinePjanova DaceZayakin PawelGerashchenko Bogdan IErenpreisa Jekaterina - Medulloblastoma (MB) is the most common childhood brain cancer, with Group 3 (G3) as the most aggressive subgroup, being prone to relapse and treatment resistance. A small subset of stem-like cells contributes to this recurrence, but the mechanisms behind their transformation are not fully understood. In this study, we employed therapeutically relevant in vitro and in vivo chemoradiotherapy (CRT) models of G3 MB and discovered a significant activation of SRC kinase following CRT treatment, while other kinases such as AKT and ERK were unaffected. Remarkably, SRC activation was exclusive to G3 MB cells and was absent in the less aggressive Sonic Hedgehog and Group 4 MB, as well as in normal brain cells. SRC activation in CRT-treated G3 MB cell and tumors corresponded with increased stemness, as evidenced by elevated levels of stemness factors SOX2, NOTCH1, OCT4, Nanog and phosphorylated STAT3, alongside a reduction in the differentiation marker βIII-tubulin/TUBB3. Conversely, SRC knockout or pharmacological inhibition promoted differentiation and reduced aggressiveness in CRT-resistant G3 MB cells, which could be rescued by re-expression of SRC in SRC knockout cells. Additionally, SRC inhibition significantly reduced the viability of CRT-treated G3 MB cells by inducing both apoptosis and necroptosis, while sparing the proliferation and stem-like properties of normal neural stem cells, indicating a promising toxicity profile. Importantly, in a therapeutically relevant orthotopic G3 MB model, administration of the re-purposed blood-brain-barrier permeable SRC inhibitor, Saracatinib, in conjunction with CRT, significantly reduced tumor burden and improved animal survival compared to CRT treatment alone without any neurotoxic side effects. Overall, our results underscore the pivotal role of SRC in enhancing stemness and aggressive behavior in CRT-resistant recurrent G3 MB. Targeting SRC not only promotes cell death through apoptosis and necroptosis but also encourages differentiation, positioning it as a promising therapeutic target for rapid clinical interventions. - Source: PubMed
Publication date: 2026/04/24
Kuzmychova HelgiChawla UjalaMartell EmmaGrewal AkaljotJain CharulRamnauth KayshanaKaul EshaSenthil HarshalVenugopal ChitraAnderson Christopher MSingh Sheila KSharif Tanveer - Spinal cord injury (SCI) results in irreversible neuronal loss, cystic cavitation, and a chronically hostile microenvironment that severely limits endogenous repair. Conventional stem cell transplantation is frequently compromised by low cell survival, uncontrolled differentiation, and rapid cell loss. To address these challenges, we developed a mechano-responsive, three-dimensional bioprinted scaffold composed of gelatin methacryloyl (GelMA) and chitosan (CS), featuring an elastic modulus of 10.0 kPa, interconnected porous architecture, and photocrosslinkable bioactivity that recapitulate key mechanical characteristics of native spinal cord tissue. When loaded with mesenchymal stem cells (MSCs), the scaffold promoted cytoplasmic sequestration of yes-associated protein (YAP), thereby directing MSC fate toward a neurogenic phenotype, accompanied by enhanced expression of stemness markers (NANOG and OCT4) and increased paracrine secretion of neurotrophic factors, including GDNF, NGF, and NT-3. In a rat complete spinal cord transection model, implantation of the MSC-laden scaffold significantly improved BBB locomotor scores and pain thresholds within 4 weeks. Histological analyses further revealed increased MAP2-positive axonal regeneration, enhanced MBP-positive myelination, and reduced GFAP-positive glial scar formation. Collectively, these findings demonstrate a scalable and effective strategy that integrates biomimetic mechanical cues with controlled stem cell fate regulation to promote functional neural regeneration following SCI. - Source: PubMed
Publication date: 2026/04/24
Luo QinglinQue XiangyongZhou YouWang MaopengZhu XiaokangWang HanJiu JingweiLi Xinzhi - Triple-negative breast cancer (TNBC) is an aggressive malignancy characterized by a high mortality rate and limited treatment options. The mechanism by which YTHDC1 contributes to TNBC progression remains to be investigated. To investigate the role of YTHDC1 in TNBC, we performed in vitro real-time quantitative polymerase chain reaction (qRT-PCR), western blot (WB), cell counting kit-8 (CCK-8), colony formation, and sphere formation assays to evaluate its impacts on TNBC cell proliferation and stemness. Fluorescence in situ hybridization (FISH) and RNA immunoprecipitation (RIP) were employed to identify the binding sites of YTHDC1 on BACH1 mRNA. The stability of BACH1 mRNA following actinomycin D (ActD) treatment was analyzed after YTHDC1 silencing. Additionally, functional assays assessed the ability of BACH1 overexpression to counteract the inhibitory effects of YTHDC1 silencing on TNBC cell proliferation and stemness. We found that YTHDC1 expression was significantly elevated in TNBC tissues and cells. Silencing YTHDC1 inhibited cell proliferation, colony formation and sphere formation, and reduced the expression of stemness markers (Nanog, Oct4, and SOX2). YTHDC1 silencing also inhibited BACH1 mRNA nuclear export, leading to an increased nucleoplasmic ratio of BACH1 mRNA. Mechanistic studies revealed that YTHDC1 and m6A modifications significantly enriched on BACH1 mRNA, while YTHDC1 silencing reduced its stability. Importantly, BACH1 overexpression rescued the inhibitory effects of YTHDC1 silencing on TNBC cell proliferation and stemness marker expression. Collectively, YTHDC1 regulates BACH1 expression in an m6A-dependent mechanism, contributing to TNBC progression. Implications: Our findings provide a rationale for further investigation of the YTHDC1/BACH1 axis as a potential therapeutic target in TNBC. - Source: PubMed
Publication date: 2026/04/24
Huang ShulinGong HaihuiXie JingYue Ou