Abstract
Purpose of Review: A growing number of studies indicate that a network of regulated cell death (RCD) pathways plays a vital role in tumorigenesis suggesting its targeting to be a promising therapeutic avenue for cancer treatment. In this review, we firstly systematically summarize the current knowledge on the impact of carrageenans on different non-conventional non-apoptotic RCDs and explore a therapeutic potential of carrageenans as RCDs-modulating agents.
Furthermore, we cover the knowledge gaps and controversies in our understanding of cell death-related carrageenan-mediated effects and highlight the directions of further research aiming at studying the pharmacological potential of carrageenans. Recent Findings: A compelling body of evidence indicates that non-apoptotic RCDs, including necroptosis, ferroptosis, pyroptosis, and autophagy-related cell death, are involved in modulating tumorigenesis and immune response in cancer.
Recent advances in our understanding of the role of distinct non-apoptotic RCDs suggest that pharmacological modulation of diverse RCDs is a tempting anti-cancer therapeutic strategy. In particular, carrageenans, which are a group of heterogenous anionic hydrocolloids of polysaccharide nature widely used as food additives (E407 and E407a), have been shown to have anti-viral, anti-cancer, and immunomodulatory activity.
The anti-cancer activity of carrageenans is attributed to a certain extent to activation of apoptosis, but the effects of carrageenan on other RCD modes, which can be targeted in oncopathology, are poorly summarized. Summary: Anti-cancer, immunomodulatory, and anti-viral properties of marine polysaccharides carrageenans are at least partly explained by their modulation of RCD modalities, primarily pyroptosis.
Thus, carrageenans can be considered promising RCD-regulating agents, which can be therapeutically exploitable. Furthermore, we emphasize the need to consider induction of non-conventional RCDs as one of the possible molecular mechanisms of carrageenan toxicity.