Extracellular matrix, via its receptors the integrins, has emerged as a crucial factor in cancer development. The α2β1 integrin is a major collagen receptor that is widely expressed and known to promote cell migration and control tissue homeostasis. Growing evidence suggests that it can be a key pathway in cancer. Recent studies have shown that α2β1 integrin is a regulator of cancer metastasis either by promoting or inhibiting the dissemination process of cancer cells. The α2β1 integrin signaling can also enhance tumor angiogenesis. Emerging evidence supports a role for α2β1 integrin in cancer chemoresistance especially in hematological malignancies originating from the T cell lineage. In addition, α2β1 integrin has been associated with cancer stem cells. In this review, we will discuss the complex role of α2β1 integrin in these processes. Collagen is a major matrix protein of the tumor microenvironment and thus, understanding how α2β1 integrin regulates cancer pathogenesis is likely to lead to new therapeutic approaches and agents for cancer treatment.
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http://dx.doi.org/10.1016/j.semcancer.2015.08.004 | DOI Listing |
Adv Wound Care (New Rochelle)
January 2025
Translational Medicine Center, Baotou Central Hospital (Baotou Clinical Medical College, Affiliated to Inner Mongolia Medical University), Baotou, China.
Wound healing is a dynamic process involving multiple cell types and signaling pathways. Dermal sheath cells (DSCs), residing surrounding hair follicles, play a critical role in tissue repair, yet their regulatory mechanisms remain unclear. This study used single-cell proteomics with the mouse model to explore DSC function across different healing stages.
View Article and Find Full Text PDFArch Endocrinol Metab
January 2025
Universidade Estadual Paulista Faculdade de Medicina de Botucatu BotucatuSP Brasil Universidade Estadual Paulista, Faculdade de Medicina de Botucatu, Botucatu, SP, Brasil.
Objective: Considering that the αvβ3 integrin plays an important role in tumor metastasis, this study investigated the involvement of these pathways in mediating the triiodothyronine (T3) effects on amphiregulin () expression.
Materials And Methods: We treated MCF-7 cells with T3 (10 nM) for 1 hour in the presence or absence of inhibitors for αvβ3 integrin (RGD peptide), MAPK (PD98059), PI3K (LY294002), and protein synthesis (cycloheximide [CHX]). A control group (C) received no T3 or inhibitors.
Adv Healthc Mater
January 2025
Department of Orthopedic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Characterized by a cascade of profound changes in nucleus pulposus (NP) cells, extracellular matrix (ECM), and biomechanics, intervertebral disc degeneration is a common multifactorial condition that may lead to various degenerative lumbar disorders. Therapeutic strategies targeting a single factor have shown limited efficacy in treating disc degeneration, and approaches that address multiple pathological ingredients are barely reported. In this study, engineered cell membrane-encapsulated keratin nanoparticles are developed to simultaneously alleviate NP cell senescence and promote ECM remodeling.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Experimental and Clinical Medicine, Section of Internal Medicine, University of Florence and Istituto Toscano Tumori (ITT), Florence, Italy.
J Am Soc Nephrol
January 2025
Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Background: Deficiency of adiponectin and its downstream signaling may contribute to the pathogenesis of kidney injury in type 2 diabetes. Adiponectin activates intracellular signaling via adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2), but the role of AdipoR-mediated signaling in glomerular injury in type 2 diabetes remains unknown.
Methods: The expression of AdipoR1 in the kidneys of people with type 2 diabetes and the expression of podocyte proteins or injury markers in the kidneys of AdipoR1-knockout (AdipoR1-KO) mice and immortalized AdipoR1-deficient human podocytes were investigated by immunohistochemistry and immunoblotting.
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