Abstract
Lung cancer is the leading cause of cancer deaths worldwide. Most of lung cancer cases are classified as non-small cell lung cancers (NSCLC). EGFR has become an important therapeutic target for the treatment of NSCLC patients, and inhibitors targeting the kinase domain of EGFR are currently used in clinical settings. Recently, an increasing interest has emerged toward understanding the mechanisms and biological consequences associated with lipid reprogramming in cancer. Increased uptake, synthesis, oxidation, or storage of lipids has been demonstrated to contribute to the growth of many types of cancer, including lung cancer. In this review, we provide an overview of metabolism in cancer and then explore in more detail the role of lipid metabolic reprogramming in lung cancer development and progression and in resistance to therapies, emphasizing its connection with EGFR signaling. In addition, we summarize the potential therapeutic approaches targeting lipid metabolism for lung cancer treatment.
Highlights
Another study [79] demonstrating the pro-apoptotic role of ceramide in lung cancer showed that treatment of non-small cell lung cancers (NSCLC) H1299 cells with exogenous C8-ceramide promoted the switch of superoxide dismutase 1 (SOD1) to SOD2, which increased the endogenous levels of reactive oxygen species (ROS), inhibiting cell proliferation and inducing apoptosis
In A549 and H1975 human lung cancer cell lines, C93 treatment triggered a protective response mediated by NF-kB signaling activation, and the pharmacological inhibition of both NF-kB and fatty acid synthase (FASN) led to more effective cell killing than inhibiting either NF-kB or FASN individually [99]
It is becoming evident that targeting a single molecule or pathway involved in lipid metabolism may not be sufficient to achieve durable suppression of cancer cell growth
Summary
One of the main alterations that takes place within cancer cells is the reprogramming of metabolism Cancer cells modify their metabolic pathways of carbohydrates, amino acids, and lipids to sustain their growth and proliferation and survive under a lack or shortage of nutrients. These changes allow them to meet the requirements of the rapid cell division and to avoid signals that would lead to their growth arrest and execution, such as apoptotic signals [7,9,10]. Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations Those associated with lipid metabolism have recently received increasing attention and recognition [11]. We shed light on the potential strategies exploiting lipid metabolism as a therapeutic target for lung cancer treatment
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
