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Pavlides, Stephanos; Tsirigos, Aristotelis; Migneco, Gemma; Whitaker-Menezes, Diana; Chiavarina, Barbara; Flomenberg, Neal; Frank, Philippe G.; Casimiro, Mathew C.; Wang, Chenguang; Pestell, Richard G.; Martinez-Outschoorn, Ubaldo E.; Howell, Anthony; Sotgia, Federica; Lisanti, Michael P.
Cell cycle (Georgetown, Tex.), 20/9/1/, Letnik: 9, Številka: 17Journal Article
A loss of stromal Cav-1 in the tumor fibroblast compartment is associated with early tumor recurrence, lymph-node metastasis, and tamoxifen-resistance, resulting in poor clincical outcome in breast cancer patients. Here, we have used Cav-1 (-/-) null mice as a pre-clinical model for this "lethal tumor micro-environment." Metabolic profiling of Cav-1 (-/-) mammary fat pads revealed the upregulation of numerous metabolites (nearly 100), indicative of a major catabolic phenotype. Our results are consistent with the induction of oxidative stress, mitochondrial dysfunction, and autophagy/mitophagy. The two most prominent metabolites that emerged from this analysis were ADMA (asymmetric dimethyl arginine) and BHB (beta-hydroxybutyrate; a ketone body), which are markers of oxidative stress and mitochondrial dysfunction, respectively. Transcriptional profiling of Cav-1 (-/-) stromal cells and human tumor stroma from breast cancer patients directly supported an association with oxidative stress, mitochondrial dysfunction, and autophagy/mitophagy, as well as ADMA and ketone production.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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