The Effect of Tissue Organization and Homeostasis on Inflammatory Cytoskeletal Signaling in Cancer

Dear Editor,

Tissue organization and homeostasis are based on a set of circuits that include inflammatory signaling that regulates the tissue environment. Imbalance of these connections may lead to inflammatory diseases and suppression of the immune system, as occurs in chronic viral infections and cancer [1]. With interferon type I (IFN-Is) as key stimuli IFN-I are produced by virus-infected cells to create an inherent cellular antiviral status in neighboring cells to eliminate infection. However, long-term IFN-I signaling leads to impaired immune function by inducing suppressive agents that impair immunity to promote tissue organization and homeostasis [2]. Imbalance of these connections may lead to inflammatory diseases and immunosuppression, as occurs in chronic viral infections and cancer, with interferon type I (IFN-Is) as key stimuli of IFN-I by cells. They become infected with the virus to create an inherent cellular antiviral status in neighboring cells to fight infection. However, long-term IFN-I signaling leads to immune dysfunction by inhibiting suppressive agents that inhibit immune enhancement [2,3].

Actin Cytoskeleton: Components, Dynamics and Emerging Role In

Actin, together with microtubules, intermediate filaments, and septin, represents the major components of the cytoskeleton of vertebrate cells, which are constantly undergoing a dynamic reorganization. Actin is present in the cell as monomeric spherical actin (G-actin) and polymer filamentous actin (F-actin). An initial complex stabilizes actin monomers and initiates polymerization, so strand formation occurs through the action of proteins such as profiles and cortactin, while polymerization is achieved by proteins such as caffeine or glycine [4]. Actin filaments can form larger structures, they interact with other actin-binding proteins, such as fasciols, or they can be cleaved by actin-binding proteins. Under the control of regulatory proteins that affect all aspects of actin strand dynamics, actin strands can be arranged to form a wide range of structures. Stress fibers are large networks of actin filaments that can cover almost the entire length of a cell, and their association with myosin causes them to contract. Cortical actin is a network of actin filaments beneath the plasma membrane. Depending on the organization, actin filaments may form cellular lesions such as lamellar podia, philopodia, microvillers, and large membrane reefs. Actin-binding proteins regulate the major signaling pathways and communicate with the genome in healthy diseases, including cancer. It is noteworthy that actin dynamics are also associated with gene transcription, and various mechanisms that link cytoplasmic action status to the nuclear genome have been described. The presence of actin in the nucleus has been clearly demonstrated, although its functional role is still debated. Gene expression is linked and increases polymerase II clustering after serum stimulation or IFNγ treatment. In addition, chromatin regulation in interferon has been reported to be essential [4].

IFN-I Signaling Mechanisms in Infection and Cancer

IFN-I is the first line of defense against viral infection and the central coordinator of inflammation in tumor microenvironments (TME). A single IFN-β protein, and IFN ε, IFN-τ, IFN-κ have been less studied., IFN-ω, IFN-δ and IFN-ζ, all of which bind to the IFN- α/β heterodimeric receptor (IFNAR) consisting of the IFNAR1 and IFNAR2 chains. IFN-I are encoded by intron-free genes on chromosome 4 in Mice and chromosome 9 in humans clustered IFN-I by all nucleated cells with involvement of different families of heterologous receptors, called pattern recognition receptors (PRRs), by pathogen-related molecular patterns (PAMPs), during infection, and molecular patterns Damage-related (DAMPs) are secreted. In cancer, PRRs are intrinsic, cytosolic, and endosolic innate immune receptors. Induction and regulation of IFN-I have been extensively studied recently and are not the focus of this study [5].

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