Autophagy is an evolutionarily conserved process in which the cell degrades its own components and recycles the biomolecules for survival and homeostasis. It is an important cellular process to eliminate pathogens or damaged organelles. Nucleophagy, also termed as nuclear autophagy, is a more recently described subtype of autophagy, in which nuclear components, such as nuclear lamina and DNA, are to be degraded. Nucleophagy plays a double-facet role in the development of cancer. On one hand, the clearance of damaged DNA or nuclear structures via autophagic pathway is crucial to maintain nuclear integrity and prevent tumorigenesis. On the other hand, in later stages of tumor growth, nucleophagy may facilitate cancer cell survival and metastasis in the nutrient-depleted microenvironment. In this review, we discuss the relationship between nucleophagy and cancer along with potential intervention methods to target cancer through manipulating nucleophagy. Given the known observations about nucleophagy, it could be promising to target different nuclear components during the processes of nucleophagy, especially nuclear lamina. Further research on investigating the role of nucleophagy in oncological context could focus on dissecting its remaining molecular pathways and their connection to known tumor suppressors.
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http://dx.doi.org/10.1002/cbin.11504 | DOI Listing |
J Neurosci Res
January 2025
Luhe Institute of Neuroscience, Capital Medical University, Beijing, China.
Despite significant advancements in achieving high recanalization rates (80%-90%) for large vessel occlusions through mechanical thrombectomy, the issue of "futile recanalization" remains a major clinical challenge. Futile recanalization occurs when over half of patients fail to experience expected symptom improvement after vessel recanalization, often resulting in severe functional impairment or death. Traditionally, this phenomenon has been attributed to inadequate blood flow and reperfusion injury.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Department of Neurology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, China.
Objective: This study aims to investigate how the E3 ubiquitin ligase LITAF influences mitochondrial autophagy by modulating MCL-1 ubiquitination, and its role in the development of epilepsy.
Methods: Employing single-cell RNA sequencing (scRNA-seq) to analyze brain tissue from epilepsy patients, along with high-throughput transcriptomics, we identified changes in gene expression. This was complemented by in vivo and in vitro experiments, including protein-protein interaction (PPI) network analysis, western blotting, and behavioral assessments in mouse models.
Glaucoma is a leading cause of irreversible blindness, often associated with elevated intraocular pressure (IOP) due to trabecular meshwork (TM) dysfunction. Diabetes mellitus (DM) is recognized as a significant risk factor for glaucoma; however, the molecular mechanisms through which hyperglycemia affects TM function remain unclear. This study investigated the impact of high glucose on gene expression in human TM (HTM) cells to uncover pathways that contribute to TM dysfunction and glaucoma pathogenesis under diabetic conditions.
View Article and Find Full Text PDFBeta-propeller Protein Associated Neurodegeneration (BPAN) is a devastating neurodevelopmental and neurodegenerative disease linked to variants in . Currently, there is no cure or disease altering treatment for this disease. This is, in part, due to a lack of insight into early phenotypes of BPAN progression and 's role in establishing and maintaining neurological function.
View Article and Find Full Text PDFUnlabelled: Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while minimizing coincidental host damage. ( ) thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. However, how protective inflammatory responses are achieved during infection and the variation of the response in different macrophage subtypes remain obscure.
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