Reprogramming of fatty acid metabolism in thyroid cancer: Potential targets and mechanisms.

Abstract

Thyroid cancer (TC) is one of the most common endocrine system tumors, and its incidence continues to increase worldwide. Although most TC patients have a good prognosis, especially with continuous advancements in surgery, radioactive iodine therapy, chemotherapy, endocrine therapy and targeted therapy, the effectiveness of disease treatment has significantly improved. However, there are still some cases with a higher risk of death and greater aggressiveness. In these more challenging advanced or highly aggressive cases, tyrosine kinase inhibitors appear to be an effective treatment option. Unfortunately, these drugs are less than ideal in terms of efficacy because of their toxicity and potential for intrinsic or acquired resistance. Therefore, exploring new strategies targeting the metabolic characteristics of TC cells and overcoming drug resistance barriers in existing treatments have become key topics in the current field of TC research. In recent years, lipid metabolic reprogramming has gained attention as an important aspect of cancer development. Lipid metabolic reprogramming not only participates in the formation of the cell membrane structure, but also plays an important role in signal transduction and promoting cell proliferation. In particular, fatty acid (FA) metabolic reprogramming has attracted widespread attention and plays an important role in multiple aspects such as tumor growth, metastasis, enhanced invasive ability, immune escape, and drug resistance. Although TC is considered a disease that is highly dependent on specific types of metabolic activities, a comprehensive understanding of the specific mechanism of action of FA metabolic reprogramming in this process is lacking. This article aims to review how FA metabolic reprogramming participates in the occurrence and development of TC, focusing on the impact of abnormal FA metabolic pathways and changes in the expression and regulation of related genes over the course of this disease. By examining the complex interactions between FA metabolic disorders and carcinogenic signaling pathways in depth, we aim to identify new therapeutic targets and develop more precise and effective treatments for TC.