Epithelial-to-mesenchymal transition (EMT) underlies cell plasticity and embryonic development and is frequently observed in advanced tumorigenesis. We demonstrated that midkine (MK), a retinoic acid-inducible heparin-binding mitogen, promotes EMT in immortalized HaCaT keratinocytes. We showed that MK binds to the Notch2 receptor in HaCaT keratinocytes. We further found that MK activates Notch2 signaling leading to protein/protein interactions between Hes1 and Jak2/Stat3 intermediates. We thus suggest that MK-induced cross talk of Notch2/Jak2/Stat3 signaling pathways can regulate cell plasticity and motility contributing to the EMT and later stages of tumorigenesis.
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http://dx.doi.org/10.4161/cc.7.11.5952 | DOI Listing |
Cell Death Dis
January 2025
Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.
Prostate cancer is a heterogeneous disease with a slow progression and a highly variable clinical outcome. The tumor suppressor genes PTEN and TP53 are frequently mutated in prostate cancer and are predictive of early metastatic dissemination and unfavorable patient outcomes. The progression of solid tumors to metastasis is often associated with increased cell plasticity, but the complex events underlying TP53-loss-induced disease aggressiveness remain incompletely understood.
View Article and Find Full Text PDFBone Res
January 2025
Jiangsu Province Key Laboratory of Oral Diseases, Nanjing, Jiangsu Province, China.
Plp1-lineage Schwann cells (SCs) of peripheral nerve play a critical role in vascular remodeling and osteogenic differentiation during the early stage of bone healing, and the abnormal plasticity of SCs would jeopardize the bone regeneration. However, how Plp1-lineage cells respond to injury and initiate the vascularized osteogenesis remains incompletely understood. Here, by employing single-cell transcriptional profiling combined with lineage-specific tracing models, we uncover that Plp1-lineage cells undergoing injury-induced glia-to-MSCs transition contributed to osteogenesis and revascularization in the initial stage of bone injury.
View Article and Find Full Text PDFCurr Opin Neurobiol
January 2025
Department of Pathology & Cell Biology, Columbia University Irving Medical Center, 10032, New York, NY, USA. Electronic address:
Neurons are equipped with microtubules of different stability with stable and dynamic domains often coexisting on the same microtubule. While dynamic microtubules undergo random transitions between disassembly and assembly, stable ones persist long enough to serve as platforms for tubulin-modifying enzymes (known as writers) that attach molecular components to the α- or β-tubulin subunits. The combination of these posttranslational modifications (PTMs) results in a "tubulin code," dictating the behavior of selected proteins (known as readers), some of which were shown to be crucial for neuronal function.
View Article and Find Full Text PDFCurr Rheumatol Rep
January 2025
Department of Rheumatology, Flinders Medical Centre, Adelaide, SA, Australia.
Purpose Of Review: Rheumatoid arthritis (RA) is a complex autoimmune disease characterized by chronic inflammation of the synovial tissue, where T cells play a central role in pathogenesis. Recent research has identified T peripheral helper (Tph) cells as critical mediators of local B cell activation in inflamed tissues. This review synthesizes the latest advancements in our understanding the of the role of T cells in RA, from initiation to established disease.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Neurology, Jinshan Hospital, Fudan University, 201508 Shanghai, China.
Background: Neuronal cholesterol deficiency may contribute to the synaptopathy observed in Alzheimer's disease (AD). However, the underlying mechanisms remain poorly understood. Intact synaptic vesicle (SV) mobility is crucial for normal synaptic function, whereas disrupted SV mobility can trigger the synaptopathy associated with AD.
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