Preliminary evidences on mitochondrial injury and impaired oxidative metabolism in breast cancer

A Novel Tumor-Suppressor, CDH18, Inhibits Glioma Cell Invasiveness Via UQCRC2 and Correlates with the Prognosis of Glioma Patients

“…It was recently reported that homozygous missense mutation in UQCRC2 might cause mitochondrial complex III deficiency, which is a relatively rare disease [28]. Putignani et al observed that the content of UQCRC2 in breast cancer cell was significantly decreased compared to that in normal epithelial cells [30,31], which is in accordance with our findings on gliomas. In recent years, a growing number of studies provided new insight into the role of mitochondria in cancer and demonstrated that impaired bioenergetic function of mitochondria is a hallmark of tumorigenesis [32,33].…”

Tumor metabolism, cancer cell transporters, and microenvironmental resistance

“…Since the 1920s the mitochondrion-cancer correlation plays a critical part of tumor biology. Otto Warburg and recent scientists have considered cancer as mitochondrial injury [13][14][15] . In particular, several studies have shown a decrease in mitochondrion number within cells [16][17][18][19] .…”

Mitochondrial free fatty acid β-oxidation supports oxidative phosphorylation and proliferation in cancer cells

“…It has been suggested that tumor cells permanently maintain an impaired oxidative phosphorylation (OxPhos) which promotes an increased glycolysis (Warburg, 1956). In consequence, OxPhos flux, and mitochondrial enzyme activities and contents are not usually determined in studies of cancer energy metabolism (Owens et al, 2011;Putignani et al, 2012). Several proposals on the possible mechanisms associated with the OxPhos impairment in cancer cells have emerged.…”