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• W2000244888 abstract "Abstract Anchorage to extracellular matrix (ECM) is essential for the execution of the mitotic program of nontransformed cells as they need simultaneous signals starting from mitogenic molecules, as growth factors (GFs), and adhesive agents belonging to ECM. Reactive oxygen species play a key function during both GF and integrin receptor signalling and are therefore recognised to have a synergistic function with several others transducers for anchorage‐dependent growth (ADG). Indeed, redox‐regulated proteins include protein tyrosine phosphatases, protein tyrosine kinases, small GTPases, cytoskeleton proteins, as well as several transcription factors. In this review, we focus on the role of reactive oxygen species (ROS) as key second messengers granting a proper executed mitosis for anchorage‐dependent cells through redox regulation of several downstream targets. Besides, redox signals elicited by ECM contact assure a protection from anoikis , a specific apoptosis induced by lack of anchorage. Cancer cells frequently show a deregulation of ROS production and a constitutive oxidative stress has been associated to the achievement of an invasive phenotype. Hence, in cancer cells, the constitutive deregulation of both mitogenic and survival pathways, likely mimicking autocrine/adhesive signals, helps to guide the transformed cells to escape the innate apoptotic response to abolish the signals started by cell/ECM contact, thus sustaining the spreading of anchorage‐independent cancer cells and the metastases growth. © 2008 IUBMB IUBMB Life, 60(5): 301–307, 2008" @default.
• W2000244888 created "2016-06-24" @default.
• W2000244888 creator A5022895279 @default.
• W2000244888 date "2008-04-17" @default.
• W2000244888 modified "2023-10-16" @default.
• W2000244888 title "From anchorage dependent proliferation to survival: Lessons from redox signalling" @default.
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• W2000244888 doi "https://doi.org/10.1002/iub.45" @default.
• W2000244888 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18421772" @default.
• W2000244888 hasPublicationYear "2008" @default.
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