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SCOPUS 학술저널

Ferroptosis and its role in gastric and colorectal cancers

Ferroptosis is a novel mechanism of programmed cell death, character-ized by intracellular iron overload, intensified lipid peroxidation, and abnormal ac-cumulation of reactive oxygen species, which ultimately resulting in cell membrane impairment and demise. Research has revealed that cancer cells exhibit a greater demand for iron compared to normal cells, indicating a potential susceptibility of cancer cells to ferroptosis. Stomach and colorectal cancers are common gastrointes-tinal malignancies, and their elevated occurrence and mortality rates render them a global health concern. Despite significant advancements in medical treatments, cer-tain unfavorable consequences and drug resistance persist. Consequently, directing attention towards the phenomenon of ferroptosis in gastric and colorectal cancers holds promise for enhancing therapeutic efficacy. This review aims to elucidate the intricate cellular metabolism associated with ferroptosis, encompassing lipid and amino acid metabolism, as well as iron metabolic processes. Furthermore, the sig-nificance of ferroptosis in the context of gastric and colorectal cancer is thoroughly examined and discussed.

INTRODUCTION

FATTY ACIDS (FAs)

FA BIOSYNTHESIS

FA CONVERSION-β-Oxidation

FA ARE CONVERTED TO TRIGLYCERIDES AND STORED IN LIPID DROPLETS

FA INSERTED INTO PL

CHOLESTEROL

LIPID PEROXIDATION

AMINO ACID METABOLISM-CYSTEINE

CYSTEINE ROUTING

GLUTAMINE

IRON METABOLISM

IRON METABOLISM REGULATION

FERROPTOSIS DEFENSE SYSTEMS

FERROPTOSIS AND GC

FERROPTOSIS AND CRC

ANTICANCER DRUGS AND ANTICANCER THERAPY RELATED TO FERROPTOSIS IN GC

ANTICANCER DRUGS AND ANTICANCER THERAPY RELATED TO FERROPTOSIS IN COLON CANCER

CONCLUSIONS

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