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J Cell Mol Med
January 2025
Department of Ophthalmology, the Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu, P. R. China.
The activation of the human interferon-inducible protein X (IFIX) isoform is associated with maintaining a stable cytoskeleton and inhibiting epithelial-mesenchymal transition (EMT). However, the mechanisms and pathways underlying IFIX-mediated oncogenesis are not well understood. In this study, we investigated the effects of IFIX overexpression and knockdown in CAL-27 and SCC-25 oral squamous cell carcinoma (OSCC) cells.
View Article and Find Full Text PDFNucleus
December 2025
Department of Physiology and Biophysics, The University of Illinois at Chicago - College of Medicine, Chicago, IL, USA.
The vascular network, uniquely sensitive to mechanical changes, translates biophysical forces into biochemical signals for vessel function. This process relies on the cell's architectural integrity, enabling uniform responses to physical stimuli. Recently, the nuclear envelope (NE) has emerged as a key regulator of vascular cell function.
View Article and Find Full Text PDFSci Rep
January 2025
Laboratory of Animal Reproduction and Development, Graduate School of Agricultural Science, Tohoku University, 468-1 Aramaki-Aoba, Aoba-Ku, Sendai, Miyagi, 980-8572, Japan.
Flagella and cilia are widely conserved motile structures, in mammalian, sperm possess flagella. Large protein complexes called dynein, including cytoplasmic dynein 2 and axonemal dynein, play a role in the formation of cilia and flagella. The function of each subunit component of dynein complexes in sperm flagellum formation remains unclear.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Internal Medicine I, Ulm University Hospital, Ulm, Germany
Background: Pancreatic ductal adenocarcinoma (PDAC) is mostly refractory to immunotherapy due to immunosuppression in the tumor microenvironment and cancer cell-intrinsic T cell tolerance mechanisms. PDAC is described as a "cold" tumor type with poor infiltration by T cells and factors leading to intratumoral T cell suppression have thus received less attention. Here, we identify a cancer cell-intrinsic mechanism that contributes to a T cell-resistant phenotype and describes potential combinatorial therapy.
View Article and Find Full Text PDFAdv Exp Med Biol
January 2025
Cancer Research UK Scotland Centre (Edinburgh), Institute of Genetics & Cancer, University of Edinburgh, Edinburgh, UK.
E-cadherin is a transmembrane protein and central component of adherens junctions (AJs). The extracellular domain of E-cadherin forms homotypic interactions with E-cadherin on adjacent cells, facilitating the formation of cell-cell adhesions, known as AJs, between neighbouring cells. The intracellular domain of E-cadherin interacts with α-, β- and p120-catenins, linking the AJs to the actin cytoskeleton.
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