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• W2005117785 endingPage "446" @default.
• W2005117785 startingPage "428" @default.
• W2005117785 abstract "•Autophagy is an intracellular recycling pathway with an emerging plastic role in cancer. •Autophagy modulates both cancer cell-autonomous and non-autonomous processes. •The interface between cancer and stromal cells autophagy models the tumor landscape. •Autophagy impacts immunosurveillance and antitumor immunity. •Understanding how autophagy modulators affect tumor stroma is key in cancer therapy. Autophagy, the major lysosomal pathway for recycling intracellular components including whole organelles, is emerging as a key process modulating tumorigenesis, tumor–stroma interactions, and cancer therapy. Research over the past decade has highlighted a context-dependent and dynamic role for autophagy in cancer: it is tumor suppressive in the early stages of cancer development, but fuels the growth of established tumors. Likewise, the stimulation of autophagy in response to therapeutics can contextually favor or weaken chemoresistance and antitumor immunity. From a therapeutic perspective, understanding whether, when, and how autophagy can be harnessed to kill cancer cells remains challenging. In this review, we discuss new connections that reveal the role of autophagy in shaping tumor–stroma interaction during carcinogenesis and in the context of anticancer treatments. Autophagy, the major lysosomal pathway for recycling intracellular components including whole organelles, is emerging as a key process modulating tumorigenesis, tumor–stroma interactions, and cancer therapy. Research over the past decade has highlighted a context-dependent and dynamic role for autophagy in cancer: it is tumor suppressive in the early stages of cancer development, but fuels the growth of established tumors. Likewise, the stimulation of autophagy in response to therapeutics can contextually favor or weaken chemoresistance and antitumor immunity. From a therapeutic perspective, understanding whether, when, and how autophagy can be harnessed to kill cancer cells remains challenging. In this review, we discuss new connections that reveal the role of autophagy in shaping tumor–stroma interaction during carcinogenesis and in the context of anticancer treatments. condition in which body fluids (e.g., blood) show an increased acidity. The shift in cellular metabolism (Warburg effect) observed in cancer cells is associated with a build-up of lactic acid, which generates a high acid load in the tumor microenvironment causing acidosis. is the induction of apoptosis by the lack of cell/extracellular matrix attachment and is a self-defense strategy that organisms use to maintain the correct position of the cells within the tissue and eliminate misplaced cells. signaling in which a cell secretes a biomolecule/factor that binds to the receptors/targets on the same cell and leads to biological changes in that cell. any process that can be initiated in its entirety by one particular cell, on its own, in response to stress/damage/stimulation. secreted chemotactic cytokine that can induce directed chemotaxis in responsive cells. small secreted protein molecules that function predominantly in immunological intercellular communication. These include interleukins (ILs) and interferons (IFNs). molecules that are normally hidden within a live cell, where they perform predominantly non-immunological functions. Following injury/stress/damage, they are emitted from the cells (surface exposed or secreted/released), and in the extracellular environment they mediate immunomodulatory processes. a cellular stress response caused by an imbalance between ER protein folding load and capacity that leads to the accumulation of unfolded proteins in the ER lumen. a complex structural entity composed of structural proteins (collagens and elastin), specialized proteins (e.g., fibronectin, fibrilin, and laminin) and proteoglycans that surrounds and supports cells to provide physical scaffolding and to initiate key biochemical and biomechanical signals necessary for tissue morphogenesis, homeostasis, and differentiation. condition in which individuals are hemizygous at a particular locus, often due to deletion of the corresponding allele, which results in a level of protein production that is insufficient for normal function. condition in which there is a deficiency in the concentration of oxygen reaching the tissues. a ‘variant’ of the physiological apoptotic cell death that is proinflammatory rather than tolerogenic. When induced in cancer cells, immunogenic cell death can mediate potent antitumor immunity. reduced or impaired activation or efficiency of the immune system. multiprotein oligomeric complex that activates various inflammatory processes due to its ability to promote the maturation of inflammatory cytokines such as IL-1β and IL-18. It is mainly expressed in myeloid cells and is an important component of the innate immune system. a complex biological response of tissues to different harmful stimuli, such as irritants, pathogens, and dying or damaged cells. Inflammation is an attempt to protect the organism by removing or eliminating the noxious stimuli and initiating the healing process. spread of tumor growth to a region remote from the site of the primary tumor. This spreading occurs via lymph or blood. a process during epithelial cancer progression through which adjacent fibroblasts become activated to proliferate and upregulate extracellular matrix production. This myofibroblastic phenotype is characterized by the acquisition of smooth muscle (SM) features, most notably contractile stress fibers and α-SM actin expression. a form of signaling in which a cell secretes a biomolecule/factor that binds to the receptors/targets on a neighboring or nearby cell, thereby leading to biological changes in that receptive cell. is the set of proteins secreted by the cells involved in intercellular communication. is a generally antiproliferative cellular process characterized by a large and flat cellular morphology, irreversible arrest of cell proliferation, and differential gene expression with upregulation of negative modulators of the cell cycle, which is commonly associated with the aging process. This antiproliferative process also acts as a strong barrier against cancer progression. specific types of cytokines that cancer cells can use as ‘growth factors’ owing to the presence of receptors on their surface that respond to these cytokines. Examples of the receptors are IL-6R and the gp130 receptor complex that initiates growth/proliferation signaling in cancer cells in response to the cytokine, IL-6." @default.
• W2005117785 created "2016-06-24" @default.
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• W2005117785 creator A5064707969 @default.
• W2005117785 creator A5073453235 @default.
• W2005117785 creator A5091862786 @default.
• W2005117785 date "2013-07-01" @default.
• W2005117785 modified "2023-10-10" @default.
• W2005117785 title "Autophagy: shaping the tumor microenvironment and therapeutic response" @default.
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