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Regulation of cerebellar neural precursor cell (NPC) death is important for both normal brain development and prevention of brain tumor formation. The tumor suppressor p53 is an important regulator of NPC apoptosis, but the precise mechanism of p53-regulated cerebellar NPC death remains largely unknown. Here, by using primary cerebellar NPCs and a mouse cerebellar NPC line, we compared the molecular regulation of cerebellar NPC death produced by staurosporine (STS), a broad-spectrum kinase inhibitor, with that caused by genotoxic agents. We found that both STS- and genotoxin-induced cerebellar NPC death were markedly inhibited by p53 or Bax deficiency. Genotoxin-induced cerebellar NPC death required new protein synthesis and PUMA, a p53 transcriptionally regulated BH3-only molecule. In contrast, STS caused cerebellar NPC death without requiring new protein synthesis or PUMA expression. In addition, genotoxic agents increased nuclear p53 immunoreactivity, whereas STS produced rapid cytoplasmic p53 accumulation. Interestingly, STS-induced death of cerebellar granule neurons was p53-independent, indicating a differentiation-dependent feature of neuronal apoptotic regulation. These results suggest that STS-induced cerebellar NPC death requires a direct effect of p53 on cytoplasmic apoptotic mediators, whereas genotoxin-induced death requires p53-dependent gene transcription of PUMA. Thus, p53 has multiple death promoting mechanisms in cerebellar NPCs.
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http://dx.doi.org/10.1097/nen.0b013e31802d4ab4 | DOI Listing |
Am J Otolaryngol
December 2024
Department of Otolaryngology, Far Eastern Memorial Hospital, New Taipei, Taiwan; Head and Neck Cancer Surveillance & Research Group, Far Eastern Memorial Hospital, New Taipei, Taiwan; Department of Electrical Engineering, Yuan Ze University, Taoyuan, Taiwan. Electronic address:
Background: Cancer has consistently been the leading cause of death worldwide, with head and neck cancer (HNC) being one of the top ten causes of cancer-related death. Nasopharyngeal carcinoma (NPC), in particular, is a cancer that is unique to East Asia. Numerous studies have shown that the Epstein-Barr virus (EBV) DNA load and the systemic immune inflammation (SII) index can serve as prognostic indicators for NPC patients.
View Article and Find Full Text PDFTransl Oncol
December 2024
Shengli Clinical Medical College of Fujian Medical University, Department of Otolaryngology, Head and Neck Surgery, Fujian Provincial Hospital, Fuzhou 350001, China. Electronic address:
Background: Nasopharyngeal carcinoma (NPC) is an epithelial malignancy with poorly understood underlying molecular mechanisms. Ferroptosis, a form of programmed cell death, is not fully elucidated in NPC.
Method: We conducted quantitative proteomics to detect dysregulated proteins in NPC tissues.
World J Oncol
December 2024
Department of Otolaryngology-Head and Neck Surgery, The Second Hospital of Jilin University, Changchun 130041, China.
Background: The effectiveness of immune checkpoint therapy highlights the need to understand abnormal programmed cell death protein-1 (PD-1) expression in nasopharyngeal carcinoma (NPC), especially when treatments fail, or resistance develops. Interferon gamma (IFN-γ) signaling is crucial for regulating programmed cell death-ligand 1 (PD-L1) expression. Our study focuses on interferon gamma receptor 2 (IFNGR2), an essential part of the IFN-γ pathway, and its impact on malignant traits in NPC.
View Article and Find Full Text PDFCell Death Discov
December 2024
Department of Oncology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Nasopharyngeal carcinoma (NPC) is a distinct type of head and neck squamous cell carcinoma prevalent in Southern China, Southeast Asia, and North Africa. Despite advances in treatment options, the prognosis for advanced NPC remains poor, underscoring the urgent need to explore its underlying mechanisms and develop novel therapeutic strategies. Epigenetic alterations have been shown to play a key role in NPC progression.
View Article and Find Full Text PDFCell Death Discov
December 2024
High Magnetic Field Laboratory, Key Laboratory of High Magnetic Field and Ion Beam Physical Biology, Chinese Academy of Sciences; Anhui Province Key Laboratory of Environmental Toxicology and Pollution Control Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, Anhui, China.
Ribonucleotide reductase M1 (RRM1), the catalytic subunit of ribonucleotide reductase, plays a pivotal role in converting ribonucleotides (NTP) into deoxyribonucleotides (dNTP), essential for DNA replication and repair. Elevated RRM1 expression is associated with various human cancers, correlating with poorer prognosis and reduced overall survival rates. Our previous study found that RRM1 will enter the nucleus to promote DNA damage repair.
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