The Bioenergetic Role of Mitochondria in Lung Cancer

Abstract

In 1920s, Otto Warburg made the observation that cancer cells utilize significantly more glucose than normal, healthy cells, which led him to believe that cancer cells relied on glycolysis more than healthy cells. However, many subsequent studies have shown that glucose is not only necessary for glycolysis but also for oxidative phosphorylation and production of building blocks for the synthesis of other molecules. There are many challenges associated with studying and treating lung cancer, and there is a diverse set of metabolic factors influencing the tumorigenesis and metastasis of lung cancer. Lung cancer cells rely heavily on mitochondrial respiration, and several studies have shown that inhibiting mitochondrial function is an effective method to combat lung cancer. Several agents have been used to inhibit mitochondrial function, including cyclopamine and metformin. Further, more research has noted increased levels of heme flux and function as critical to intensified oxygen consumption and accompanying amplified pathogenesis and progression of lung cancer. The upregulation of mitochondrial DNA and biogenesis genes are also correlated with lung cancer. In this chapter, we will cover these recent and emerging topics in lung cancer bioenergetics research.

Clinicopathological significance of unraveling mitochondrial pathway alterations in non‐small‐cell lung cancer

“…Thus, there is a dire need for the development of new biomarkers and therapeutic strategies for better LC management. Reprogramming of mitochondrial bioenergetics plays a critical role in lung tumorigenesis 20 . Identification and characterization of the LC‐associated critical mitochondrial alteration pathways may potentially lead to the development of novel detection/monitoring and therapeutic strategies.…”