Ferroptosis, a unique modality of cell death, caused by iron-dependent peroxidation of phospholipids on cell membranes, which is different from apoptosis, necrosis, and autophagy. Ferroptosis is closely related to a number of disease progressions, including cancers. Recent discoveries have focused on alterations that occur in lipid metabolism during ferroptosis and have provided intriguing insights into the interplay between ferroptosis and lipid metabolism in cancers. Their interaction regulates the initiation, development, metastasis, therapeutic resistance of cancer, as well as the tumour immunity, which offers several potential strategies for cancer treatment. Several studies have shown that ferroptosis leads to mitochondrial dysfunction and toxic lipid peroxidation in cells, which plays a pivotal role in suppressing cancer cell growth and progression. Although these studies have reported many tumor-associated genes influencing cell ferroptosis, such as TP53, BAP1, and Ras, there are still many tumor ferroptosis associated genes and their related signalling pathways that have not been discovered and remain to be explored.
We welcome to contributions in the form of Original Research Articles, Reviews, and Mini-Reviews that cover but are not limited to the following topics related to ferroptosis in cancer:
* The current molecular mechanisms and regulatory networks of ferroptosis
* The potential physiological functions of ferroptosis in tumour suppression and immune surveillance.
*The effect of ferroptosis on cellular metabolism and the tumor microenvironment (TME).
*The regulatory mechanism of ferroptosis and its association with several pathways, including iron, lipid, and cysteine metabolism.
*Ferroptosis and tumor drug resistance.
Please note: The findings based on data integration should be also validated by observational/experimental data. Descriptive studies and studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic data do not fall within the scope of the journal.
Ferroptosis, a unique modality of cell death, caused by iron-dependent peroxidation of phospholipids on cell membranes, which is different from apoptosis, necrosis, and autophagy. Ferroptosis is closely related to a number of disease progressions, including cancers. Recent discoveries have focused on alterations that occur in lipid metabolism during ferroptosis and have provided intriguing insights into the interplay between ferroptosis and lipid metabolism in cancers. Their interaction regulates the initiation, development, metastasis, therapeutic resistance of cancer, as well as the tumour immunity, which offers several potential strategies for cancer treatment. Several studies have shown that ferroptosis leads to mitochondrial dysfunction and toxic lipid peroxidation in cells, which plays a pivotal role in suppressing cancer cell growth and progression. Although these studies have reported many tumor-associated genes influencing cell ferroptosis, such as TP53, BAP1, and Ras, there are still many tumor ferroptosis associated genes and their related signalling pathways that have not been discovered and remain to be explored.
We welcome to contributions in the form of Original Research Articles, Reviews, and Mini-Reviews that cover but are not limited to the following topics related to ferroptosis in cancer:
* The current molecular mechanisms and regulatory networks of ferroptosis
* The potential physiological functions of ferroptosis in tumour suppression and immune surveillance.
*The effect of ferroptosis on cellular metabolism and the tumor microenvironment (TME).
*The regulatory mechanism of ferroptosis and its association with several pathways, including iron, lipid, and cysteine metabolism.
*Ferroptosis and tumor drug resistance.
Please note: The findings based on data integration should be also validated by observational/experimental data. Descriptive studies and studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic data do not fall within the scope of the journal.
