A5064761693- Epigenetics and DNA Methylation
- Pluripotent Stem Cells Research
- Mitochondrial Function and Pathology
- Chromatin Remodeling and Cancer
- Cancer Genomics and Diagnostics
- Histone Deacetylase Inhibitors Research
- Glioma Diagnosis and Treatment
- Protein Degradation and Inhibitors
- Autophagy in Disease and Therapy
- RNA Research and Splicing
- Cancer, Hypoxia, and Metabolism
- Brain Tumor Detection and Classification
- Molecular Biology Techniques and Applications
- Synthesis of Organic Compounds
- Phytochemistry and biological activity of medicinal plants
- interferon and immune responses
- Computational Drug Discovery Methods
- MicroRNA in disease regulation
- Synthesis and biological activity
- Cytokine Signaling Pathways and Interactions
- RNA modifications and cancer
- Tea Polyphenols and Effects
- Drug-Induced Hepatotoxicity and Protection
- Cancer-related molecular mechanisms research
- RNA and protein synthesis mechanisms
National Center of Biomedical Analysis
2019-2025
Capital Medical University
2025
Low levels of reactive oxygen species (ROS) are crucial for maintaining cancer stem cells (CSCs) and their ability to resist therapy, but the ROS regulatory mechanisms in CSCs remains be explored. Here, we discover that prohibitin (PHB) specifically regulates mitochondrial production glioma stem-like (GSCs) facilitates GSC radiotherapeutic resistance. We find PHB is upregulated GSCs associated with malignant gliomas progression poor prognosis. binds peroxiredoxin3 (PRDX3), a...
Type I interferons (IFNs) are known to mediate antineoplastic effects during tumor progression. IFNs can be produced by multiple cell types in the microenvironment; however, molecular mechanisms which cells evade inhibition of immune microenvironment remain unknown. Here we demonstrate that glioma stem-like (GSCs) type IFN suppression through downregulation STAT1 initiate growth under inhospitable conditions. The is mediated MBD3, an epigenetic regulator. MBD3 preferentially expressed GSCs...
<p>Supplementary Figures S1 shows that GSCs produce high levels of phosphocreatine through upregulating CKB. Supplementary S2 ZEB1 promotes CKB transcription in GSCs. S3 knockdown impedes GBM growth. S4 disruption production S5 cCr treatment no side effect on mice. S6 binds to BRD2 and inhibits its ubiquitin mediated proteasomal degradation. S7 chromosome segregation GSC proliferation transcription. S8 biosynthesis by improves JQ1 therapeutic efficacy GBM.</p>
The infiltration of glioblastoma multiforme (GBM) is predominantly characterized by diffuse spread, contributing significantly to therapy resistance and recurrence GBM. In this study, we reveal that microtubule deacetylation, mediated through the downregulation fibronectin type III SPRY domain-containing 1 (FSD1), plays a pivotal role in promoting GBM infiltration. FSD1 directly interacts with histone deacetylase 6 (HDAC6) at its second catalytic domain, thereby impeding activity on...
<p>Supplementary Figures S1 shows that GSCs produce high levels of phosphocreatine through upregulating CKB. Supplementary S2 ZEB1 promotes CKB transcription in GSCs. S3 knockdown impedes GBM growth. S4 disruption production S5 cCr treatment no side effect on mice. S6 binds to BRD2 and inhibits its ubiquitin mediated proteasomal degradation. S7 chromosome segregation GSC proliferation transcription. S8 biosynthesis by improves JQ1 therapeutic efficacy GBM.</p>
Abstract Background The previous research has confirmed the existence of idiosyncratic drug-induced liver injury (IDILI) caused by Polygonum multiflorum (PM-IDILI), and demonstrated that PM-IDILI is an immune-mediated injury, with HLA-B*35:01 identified as a genetic susceptibility marker. Additionally, emodin-8- O-β -D-glucoside (EG) 2,3,5,4′-tetrahydroxystilbene-2- have been proposed potential contributory ingredients in pathogenesis PM-IDILI. However, precise mechanisms through which these...
A series of benzo[a]pyrano[2,3-c]phenazine derivatives with a wide range substitutions at ring C the benzophenazine were designed and synthesized using one-pot, four-component domino reactions. The targeted compounds evaluated for their antitumor activities against HCT116, MCF7, HepG2 A549 cancer cell lines in vitro. most active compound 6{1,2,1,9} featured CN p-dimethylamino phenyl substituents on γ-pyran structure C. Significantly, was found to have highest growth inhibitory activity line...
Glioblastoma (GBM) exhibits profound metabolic plasticity for survival and therapeutic resistance, while the underlying mechanisms remain unclear. Here, we show that GBM stem cells reprogram epigenetic landscape by producing substantial amounts of phosphocreatine (PCr). This production is attributed to elevated transcription brain-type creatine kinase, mediated Zinc finger E-box binding homeobox 1. PCr inhibits poly-ubiquitination chromatin regulator bromodomain containing protein 2 (BRD2)...
Glioma stem-like cells (GSCs) are a subset of tumor that initiate malignant growth and promote the therapeutic resistance glioblastoma, most lethal primary brain tumor. Ribosome biogenesis is an essential cellular process to maintain cell growth, but its regulatory mechanism in GSCs remains largely unknown. Here, we show WD repeat domain 12 (WDR12), component Pes1-Bop1 complex (PeBoW), required for ribosome GSCs. WDR12 preferentially expressed compared non-stem normal cells. High levels...
<p>Supplementary Figures S1 shows that GSCs produce high levels of phosphocreatine through upregulating CKB. Supplementary S2 ZEB1 promotes CKB transcription in GSCs. S3 knockdown impedes GBM growth. S4 disruption production S5 cCr treatment no side effect on mice. S6 binds to BRD2 and inhibits its ubiquitin mediated proteasomal degradation. S7 chromosome segregation GSC proliferation transcription. S8 biosynthesis by improves JQ1 therapeutic efficacy GBM.</p>