Integrins are a large family of heterodimeric cell adhesion molecules composed of α and β subunits. Through interaction with their specific ligands, integrins mediate cell-cell and cell-extracellular matrix interactions. Via outside-in signaling, integrins can recruit cytoplasmic proteins to their intracellular domains and then cluster into supramolecular structures and trigger downstream signaling. Integrin activation is associated with a global conformation rearrangement from bent to extended in ectodomains and the separation of α and β subunit cytoplasmic domains. During cell migration, integrins regulate the focal adhesion dynamics and transmit forces between the extracellular matrix and the cell cytoskeleton. In tumor microenvironment, integrins on multiple kinds of cells could be activated, which modulates cell migration into tumor and contributes to angiogenesis and tumor metastasis. Here, we review the mechanism of integrin activation, dynamics of focal adhesions during cell migration and tumor metastasis.
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BMC Gastroenterol
January 2025
Department of General Surgery, The Second Affiliated Hospital of Jiaxing University, Zhejiang Province, Jiaxing, 314000, China.
Background: Pancreatic adenocarcinoma (PAAD) is a common malignancy with a very low survival rate. More and more studies have shown that SPTAN1 may be involved in the development and progression of a variety of tumors, including rectal cancer, Pancreatic adenocarcinoma, etc., and may affect their prognosis.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Orthopaedics, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei Province, China.
Osteosarcoma (OS) is a prevalent invasive bone cancer, with numerous homeobox family genes implicated in tumor progression. This study aimed to develop a prognostic model using HOX family genes to assess osteosarcoma patient outcomes. Data from osteosarcoma patients in The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) cohorts were collected.
View Article and Find Full Text PDFSci Rep
January 2025
Children's Research Center, Division of Oncology, University Children's Hospital Zürich, Zürich, Switzerland.
De-regulated protein expression contributes to tumor growth and progression in medulloblastoma (MB), the most common malignant brain tumor in children. MB is associated with impaired differentiation of specific neural progenitors, suggesting that the deregulation of proteins involved in neural physiology could contribute to the transformed phenotype in MB. Calsynthenin 1 (CLSTN1) is a neuronal protein involved in cell-cell interaction, vesicle trafficking, and synaptic signaling.
View Article and Find Full Text PDFBioconjug Chem
January 2025
Institute of Biochemistry, University of Münster, Corrensstraße 36, 48149 Münster, Germany.
Inflammation is a dynamic process which importantly involves migration of immune cells. Understanding the onset, acute phase and resolution of inflammation is greatly facilitated by their imaging. However, immune cells are sensitive, difficult to genetically manipulate and prone to changes in response to contact, hindering the application of well-established cell labeling methods.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Qingdao Key Laboratory of Materials for Tissue Repair and Rehabilitation, School of Rehabilitation Sciences and Engineering, University of Health and Rehabilitation Sciences, Qingdao, Shandong, People's Republic of China
Background: Tumor cells can drive the senescence of effector T cells by unbalancing their lipid metabolism, thereby limiting adoptive T cell therapy and contributing to tumor immune evasion. Our objective is to provide a feasible strategy for enhancing T cell treatment efficacy against solid tumors.
Methods: In this study, liposomal arachidonyl trifluoromethyl ketone (ATK) was anchored onto the adoptive T cell surface via bioorthogonal reactions, aiming to specifically inhibit the group IVA cytosolic phospholipase Aα (cPLAα), a key enzyme facilitating phospholipid metabolism and senescent state of T cells.
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