Ferroptosis is a recently identified form of non-apoptotic regulated cell death
with distinct properties and several functions involved in physical conditions or various
diseases. It has been related to the pathological cell death associated with degenerative
diseases (i.e., Alzheimer's, Huntington's and Parkinson's diseases), carcinogenesis,
stroke, intracerebral haemorrhage, traumatic brain injury, ischemia-reperfusion injury,
and kidney degeneration.
This entity is characterised by an iron-dependent accumulation of lipid peroxides, and
it can be induced by experimental compounds and clinical drugs in cancer cells as well
as certain normal cells. Some of the inductors are erastin, Ras-selective lethal small
molecules (RSL3 and RSL5), buthionine sulfoximine, acetaminophen, ferroptosisinducing
agents, lanperisone, sulfasalazine, sorafenib, and artesunate.
Induction of ferroptosis by drugs has been shown to inhibit cancer cell growth, both in
Ras-dependent and Ras-independent forms. This fact suggests that cancer cells display
genetic heterogeneity in the timing of the ferroptosis response.
Malignant haematological entities have been subject to a wide variety of available
treatments. However, the development of resistance to chemotherapeutic agents
represents one of the biggest obstacles in the effectiveness of the treatment of some
haematological neoplasms such as acute myeloid leukaemia. Ferroptosis has the
potential to modify the course of treatment, and hence the prognosis, not only of acute
myeloid leukaemia but also of diffuse large B-cell lymphoma, T-lymph coelom and
myeloma.
An improved understanding of the role of ferroptosis in cancer and injury-associated
diseases will create a new opportunity for diagnosis and therapeutic intervention.
Keywords: Apoptosis, Autophagy, Cancers, Ferroptosis, GPX4.
