A Review on the Antimutagenic and Anticancer Effects of Cysteamine

Abstract

Cancer is one of the leading causes of death worldwide. First-line treatments usually include surgery, radiotherapy, and/or systemic therapy. These methods can be associated with serious adverse events and can be toxic to healthy cells. Despite the new advances in cancer therapies, there is still a continuous need for safe and effective therapeutic agents. Cysteamine is an aminothiol endogenously synthetized by human cells during the degradation of coenzyme-A. It has been safely used in humans for the treatment of several pathologies including cystinosis and neurodegenerative diseases. Cysteamine has been shown to be a potent antimutagenic, anticarcinogenic, and antimelanoma in various in vitro and in vivo studies, but a review on these aspects of cysteamine’s use in medicine is lacking in the current literature. The efficacy of cysteamine has been shown in vitro and in vivo for the treatment of different types of cancer, such as gastrointestinal cancer, pancreatic cancer, sarcomas, hepatocellular carcinoma, and melanoma, leading to the significant reduction of lesions and/or the increase of survival time. Although the mechanisms of action are not fully understood, possible explanations are (i) free radical scavenging, (ii) alteration of the tumor cell proliferation by affecting nucleic acid and protein synthesis or inhibition of DNA synthesis, and (iii) hormone regulation. In conclusion, regarding the high safety profile of cysteamine and the current literature data presented in this article, cysteamine might be considered as an interesting molecule for the prevention and the treatment of cancer. Further clinical studies should be performed to support these data in humans.

Cysteamine HCl Administration Impedes Motor and Olfactory Functions, Accompanied by a Reduced Number of Dopaminergic Neurons, in Experimental Mice: A Preclinical Mimetic Relevant to Parkinson’s Disease

“…The Cys-HCl administration-induced reduction in antioxidants in experimental brains has become increasingly evident [18]. The anticancer effect of Cys-HCl has been reported to be associated with mitochondrial degeneration linked to the accumulation of iron, and this event activates peroxidase-positive autophagosomes, ultimately leading to cell death [46,47]. Considering these facts, it has been proposed that Cys-HCl induces iron-dependent, lipid peroxidation-driven ferroptosis, a mechanism that could be linked to the neurodegenerative processes observed in PD [48].…”

Cysteamine HCl Administration Impedes Motor and Olfactory Functions Accompanied by Reduced Dopaminergic Neurons in Experimental Mice: A Preclinical Mimetics Relevance to Parkinson’s Disease

“…Meantime, cysteamine administrationinduced reduction of antioxidants in the experimental brains has become incorrectly evident [27]. The anticancer effect of cysteamine has been reported to be associated with mitochondrial degeneration linked to the accumulation of iron and this event activates peroxidase-positive autophagosomes, ultimately leading to cell death [40,41]. Considering these facts, cysteamine HCl can be proposed to induce iron-dependent, lipid peroxidation-driven ferroptosis, a mechanism that could be linked to the neurodegenerative processes observed in PD [42].…”