User:LoganSlade

Logan Slade
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Early life
words to avoid filter Glutamine is the most abundant free amino acid in the blood and a main physiological source of nitrogen in mammalian cells.4,5 Nevertheless, despite being a nonessential amino acid from a biochemical point of view, glutamine becomes physiologically essential in conditions of high proliferation.21 The increased consumption of glutamine has been linked to the dysregulation of oncogenes and tumor suppressors.22,23 Thus, Wise et al. 22 in 2008 described the finding that MYC increases the expression of the cellular transporter of glutamine, and enhances the consumption of glutamine in cancer cells. Through glutaminolysis, glutamine is first deamidated to glutamate, in an irreversible reaction catalyzed by the enzyme GLS (glutaminase). Then, glutamate is further deaminated to αKG by the enzyme GLUD1/GLUD (glutamate dehydrogenase) (Fig. 1).9 GLS exists in 2 isoforms, GLS/GLS1/KGA (the kidney-type) and GLS2/LGA (the liver-type), encoded by the genes GLS and GLS2, respectively.24 GLS, which is the isoform that mainly accounts for the glutaminase activity of tumor cells, is inhibited by glutamate and is distributed ubiquitously.25,26 In contrast, GLS2 is mainly expressed in the liver and cannot be inhibited by glutamate.24,25,27 Additionally, whereas GLS2 is activated by ammonium, GLS is not.28,29 As glutamate levels regulate the activity of GLS, the production of αKG through glutaminolysis also requires an increase in the activity of GLUD1. Importantly, leucine, a key

Middle Life
Metastatic breast cancer is an incurable disease, often characterized by poor response to standard chemotherapy, which is mainly based on anthracyclines and taxanes. Thus, increasing tumor cell sensitivity to these agents is an attractive goal towards improving the clinical management of this disease. The present study investigates the effects of signal transducer and activator of transcription 3 (Stat3) inhibition on the response of the highly metastatic MDA-MB-231 human breast adenocarcinoma cell line to doxorubicin (DOX). Stat3 is a transcription factor often constitutively activated in breast tumors and cancer cell lines, and is thought to contribute to malignant transformation and progression by transactivation of a host of target genes involved in cell proliferation and survival, angiogenesis and invasiveness. Our results indicate that (a) untreated MDA-MB-231 cells express higher baseline levels of (activated) pTyr(705)Stat3, that are further upregulated following exposure to DOX, than the non-metastatic MCF-7 cell line; (b) inhibiting the Stat3 signaling pathway, by exposure to the tyrphostin AG490 (an inhibitor of the upstream activating Janus kinases), by transfection with a dominant-negative form of Stat3 or by treatment with satraplatin (a tetravalent platinum derivative that inhibits Stat3 activation), increases breast cancer cell response to the proapoptotic effect of DOX (to different extents). In addition, the latter two approaches have been shown to interfere with expression of one or more antiapoptotic proteins. Overall, these observations suggest that suppression of Stat3 signaling may provide a potential therapeutic approach to overcoming DOX resistance in metastatic breast cancer cells.