The Role of Toll-Like Receptors in Oncotherapy

Abstract

Toll-like receptors (TLRs) are associated with tumor growth and immunosuppression, as well as apoptosis and immune system activation. TLRs can activate apoptosis and innate and adaptive immunity pathways, which can be pharmacologically targeted for the development of anticancer oncotherapies. Several studies and clinical trials indicate that TLR agonists are promising adjuvants or elements of novel therapies, particularly when used in conjunction with chemotherapy or radiotherapy. An increasing number of studies suggest that the activation of TLRs in various cancer types is related to oncotherapy; however, before this finding can be applied to clinical practice, additional studies are required. Research suggests that TLR agonists may have potential applications in cancer therapy; nevertheless, because TLR signaling can also promote tumorigenesis, a critical and comprehensive evaluation of TLR action is warranted. This review focuses on recent studies that have assessed the strengths and weaknesses of utilizing TLR agonists as potential anticancer agents.

Galectin-3 in Inflammasome Activation and Primary Biliary Cholangitis Development

“…Inflammasome activation plays an important role in the pathogenesis of liver diseases (metabolic and inflammatory) that are triggered by weak but repetitive stimuli. On the other hand, strong stimulators of the immune system used in the induction of autoimmune hepatitis activate primarily innate immunity receptors [ 156 ]. N. aromaticivorans is bacteria with an atypical cell wall containing glycosphingolipids, molecules similar to molecules in the eukaryotic membrane, which generally do not cause inflammation and tissue damage, although it is detected in the mucosa of the digestive tract [ 157 ].…”

The Challenge of the Sponge Suberites domuncula (Olivi, 1792) in the Presence of a Symbiotic Bacterium and a Pathogen Bacterium

“…The Bcl-2 family is composed of pro- and anti-apoptotic molecules activated by extrinsic and intrinsic apoptotic signals [32] including those transmitted by TLRs [33]. Sponge Bcl-2 homologous Protein (BHP) has a high similarity to some mammalian Bcl-2 members and some of these molecules confer resistance against induction of apoptosis.…”

Chemotherapy-Induced Intestinal Microbiota Dysbiosis Impairs Mucosal Homeostasis by Modulating Toll-like Receptor Signaling Pathways

“…They can recognize pathogen-associated molecular patterns on various microbes (such as peptidoglycan, lipopolysaccharide (LPS), lipoteichoic acid, etc.) and the damage-associated molecular patterns from stressed or dying cells [45]. TLRs are expressed throughout the whole intestinal tract by a wide variety of cell types, including intestinal epithelial cells, fibroblasts, macrophages, neutrophils and dendritic cells [46,47].…”

“…In general, TLRs could activate the MyD88-dependent pathway (except TLR-3) and the MyD88-independent TRIF/TRAM pathway (TLR-3 and some TLR-4 signals) [45]. MyD88dependent pathway activation results in the synthesis of proinflammatory cytokines and mediates inflammatory responses.…”