Mitochondria “fuel” breast cancer metabolism: Fifteen markers of mitochondrial biogenesis label epithelial cancer cells, but are excluded from adjacent stromal cells

JNK1 stress signaling is hyper-activated in high breast density and the tumor stroma: Connecting fibrosis, inflammation, and stemness for cancer prevention

“…In addition, genetic ablation of JNK (−/−) or pharmacological inhibition of JNK-activity (with SP-600125) are both sufficient to dramatically impair wound closure by dermal fibroblasts by inhibiting cell motility/migration. 14 The HD fibroblast gene signature shares many functional similarities with the cancer-associated fibroblast (CAF) phenotype Consistent with the idea that HD fibroblasts may possess a CAF-like phenotype, HD fibroblasts overexpress the same classes of markers that are found in CAFs [15][16][17][18][19][20][21] (Table 5), including PDPN and CDH11. More specifically, many of these CAF-markers are functionally related to matrix remodeling, autophagy, senescence, ketone production, hypoxia, oxidative stress, inflammation, DNA damage, and stemness, 22 as well as FGF/EGF/PDGF-signaling.…”

Structure and Function of the Mitochondrial Ribosome

“…Mitochondrial ribosomes have been intensively investigated due to their unique structure and composition and also due to their involvement in human pathologies (38)(39)(40), including cardiomyopathies and developmental abnormalities (39,(41)(42)(43)(44)(45), cancer (46)(47)(48), and hearing loss (ototoxicity) (49). The latter is exacerbated in patients who bear sensitizing mutations in the mitochondrial rRNAs (50), which occur in roughly 0.2-0.3% of the population (51)(52)(53).…”

Phosphatase and Tensin Homolog Deleted on Chromosome 10 (PTEN) Signaling Regulates Mitochondrial Biogenesis and Respiration via Estrogen-related Receptor α (ERRα)

“…Enhanced mitochondrial function is also not uncommon in tumors (5)(6)(7). Particularly, recent evidence using immunohistochemistry and laser dissection suggests that tumor cells are highly dependent on mitochondrial respiration, whereas the surrounding stromas often rely on glycolytic respiration with low expression of mitochondrial genes (8,9). One consequence of the enhanced mitochondrial respiration is the buildup of reactive oxygen species (ROS), 2 the byproduct of mitochondrial respiration and oxidative phosphorylation.…”