PTEN is a lipid phosphatase, and PTEN mutations are associated with gliomas, macrocephaly, and mental deficiencies. We have used PTEN +/- mice to assess PTEN's role in subventricular zone (SVZ) precursor cells. For cultured SVZ neurosphere cells, haploinsufficiency for PTEN increases phosphorylation of Akt and forkhead transcription factor and slightly enhances proliferation. Based on a filter penetration assay, PTEN +/- cells are substantially more migratory and invasive than +/+ cells. The +/- cells also are more resistant to H(2)O(2)-induced apoptosis. Analysis of PTEN +/- and +/+ mice by BrdU labeling reveals no difference in the rate of cell proliferation in the SVZ. Exit of BrdU-labeled cells from the SVZ and radial migration to the outer layers of the olfactory bulb are more rapid for +/- cells. These observations indicate that PTEN regulates SVZ precursor cell function and is particularly important for migration and apoptosis in response to oxidative stress.
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http://dx.doi.org/10.1006/mcne.2002.1115 | DOI Listing |
Purpose: In glioblastoma, the therapeutically intractable and resistant phenotypes can be derived from glioma stem cells, which often have different underlying mechanisms from non-stem glioma cells. Aberrant signaling across the EGFR-PTEN-AKT-mTOR pathways have been shown as common drivers of glioblastoma. Revealing the inter and intra-cellular heterogeneity within glioma stem cell populations in relations to signaling patterns through these pathways may be key to precision diagnostic and therapeutic targeting of these cells.
View Article and Find Full Text PDFDis Model Mech
January 2025
Department of Radiology, University of Illinois at Chicago, Chicago, IL, USA.
Hepatocellular carcinoma (HCC) is an aggressive disease with poor prognosis, necessitating preclinical models for evaluating novel therapies. Large animal models are particularly valuable for assessing locoregional therapies, which are widely employed across HCC stages. This study aimed to develop a large animal HCC model with tailored tumor mutations.
View Article and Find Full Text PDFMol Med
January 2025
Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, China.
Background: Mitochondrial dysfunction and neuronal damage are major sign of cytopathology in Huntington's disease (HD), a neurodegenerative disease. Ubiquitin specific peptidase 11 (USP11) is a deubiquitinating enzyme involved in various physiological processes through regulating protein degradation. However, its specific role in HD is unclear.
View Article and Find Full Text PDFCir Cir
January 2025
Department of Genetics, Kocaeli University, Faculty of Medicine, Kocaeli, Turkey.
Objective: Understanding the relationship between genetic structure and the molecular changes involved in endometrial cancer (EC) provides an opportunity to personalize treatments and incorporate targeted therapies.
Method: We compared cytogenetic and molecular features observed in tumoral and adjacent healthy tissue endometrium samples in EC patients.
Results: Non-clonal chromosome aberrations (NCCAs) frequently in patients with EC, especially in 10,15,17,22, X chromosomes and were monitored in 73.
Hepatol Commun
January 2025
Department of Gastroenterology, The First Hospital of China Medical University, Shenyang, PR China.
Objective: Accumulating evidence suggests that microRNAs derived from macrophage exosomes can regulate the stemness and progression of cancer. However, the interaction mechanisms between HCC cells and tumor-associated macrophages remain unclear.
Methods: Exosomes were extracted from control or CD63 overexpression macrophages and co-cultured with HCC cells.
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