gp38k (CHI3L1) is a secreted heparin-binding glycoprotein whose expression, in vitro, is associated with vascular smooth muscle cell (VSMC) migration and invasion into the underlying gelatinous matrix. gp38k is expressed at high levels in postconfluent "nodular" VSMC cultures and at low levels in subconfluent proliferating cultures. In vivo, expression of gp38k homologs is high in regions of tissue remodeling and now has been detected in atherosclerotic plaques and in the developing heart. We tested the hypothesis that gp38k functions to modulate VSMC adhesion and migration. By use of modified Boyden chambers, gp38k at a concentration as low as 1 ng/ml has profound effects on VSMC migration but little or no effect on fibroblast migration. In addition, gp38k adsorbed to polystyrene surfaces directly promotes VSMC attachment and spreading. Attachment is inhibited in the presence of affinity-purified anti-gp38k or 10 mM EDTA. These results establish that gp38k is a new vascular cell adhesion and migration factor that may have a role in processes leading to vascular occlusion and heart development. gp38k may interact with VSMC via an EDTA-sensitive mechanism consistent with integrin mediated cell-matrix interaction.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s0014-4827(03)00069-7 | DOI Listing |
Haematologica
March 2025
Experimental Hematology, Vall d'Hebron Institute of Oncology (VHIO), Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain; Department of Medicine, Universitat Autònoma de Barcelona, Bellaterra.
Continuous treatment with ibrutinib not only exerts tumor control but also enhances T cell function in patients with chronic lymphocytic leukemia (CLL). We conducted longitudinal multi-omics analyses in samples from CLL patients receiving ibrutinib upfront to identify potential adaptive mechanisms to Bruton tyrosine kinase (BTK) inhibition during the first 12 months of continuous therapy. We found that ibrutinib induced a decrease in the expression of exhaustion markers and the proportion of Tregs and Tfh cells normalized to levels observed in healthy donors.
View Article and Find Full Text PDFInt J Mol Sci
February 2025
Institute of Physics, Faculty of Physics, Astronomy and Applied Computer Science, Jagiellonian University, 30-348 Kraków, Poland.
Cancer is the second most common cause of death in the world, representing one of the main economic burdens in health care and research. The effort of research has mainly focused on limiting the growth of a localized tumor, but most recently, there has been more attention focused on restricting the spreading of the cancer via invasion and metastasis. The signaling pathways behind these two processes share many molecules with physiological pathways regulating cell adhesion and migration, and, moreover, adhesion and migration processes themselves underlie tumor potential for invasion.
View Article and Find Full Text PDFMolecules
February 2025
State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300350, China.
Cancer remains a significant global public health challenge, with hepatocellular carcinoma (HCC) ranking among the top five malignancies in terms of mortality. Faberidilactone A, a sesquiterpenoid dimer isolated from , exhibits potent cytotoxicity against various human tumor cell lines and demonstrates remarkable antitumor potential. In vitro studies using HepG2 cells revealed that faberidilactone A induces apoptosis and ferroptosis, causes cell cycle arrest, enhances the production of intracellular reactive oxygen species (ROS), and disrupts mitochondrial function.
View Article and Find Full Text PDFCancers (Basel)
February 2025
Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
NINJ1 was initially recognized for its role in nerve regeneration and cellular adhesion. Subsequent studies have uncovered its participation in cancer progression, where NINJ1 regulates critical steps in tumor metastasis, such as cell migration and invasion. More recently, NINJ1 has emerged as a multifunctional protein mediating plasma membrane rupture (PMR) in several lytic cell death processes, including apoptosis, necroptosis, and pyroptosis.
View Article and Find Full Text PDFCancers (Basel)
February 2025
Division of General and Transplant Surgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 704, Taiwan.
Background/objectives: The post-hepatectomy survival of patients with hepatocellular carcinoma (HCC) faces challenges due to high recurrence rates, especially early recurrence (ER). We investigated DNA methylation in HCC and developed a methylation-based model for ER prediction (MER).
Methods: We studied HCC patients with ER within a year post-hepatectomy, comparing them to those who remained recurrence-free (RF) for 5 years.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!