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Natalia Scaglia

Researcher at National University of La Plata

Publications -  14
Citations -  1055

Natalia Scaglia is an academic researcher from National University of La Plata. The author has contributed to research in topics: Lipogenesis & Lipid metabolism. The author has an hindex of 10, co-authored 13 publications receiving 877 citations. Previous affiliations of Natalia Scaglia include Rutgers University & Harvard University.

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Inhibition of stearoylCoA desaturase-1 inactivates acetyl-CoA carboxylase and impairs proliferation in cancer cells: role of AMPK.

TL;DR: The data suggest that cancer cells require active SCD1 to control the rate of glucose-mediated lipogenesis, and that whenSCD1 activity is impaired cells downregulate SFA synthesis via AMPK-mediated inactivation of acetyl-CoA carboxylase, thus preventing the harmful effects of SFA accumulation.
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A novel direct activator of AMPK inhibits prostate cancer growth by blocking lipogenesis

TL;DR: It is shown that direct activation of AMPK inhibits PCa cell growth in androgen sensitive and castration resistant PCa (CRPC) models, induces mitotic arrest, and apoptosis, and it is demonstrated that MT 63–78 enhances the growth inhibitory effect of AR signaling inhibitors MDV3100 and abiraterone.
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Stearoyl-COA desaturase is involved in the control of proliferation, anchorage-independent growth and survival in human transformed cells

TL;DR: The data suggest that, by globally regulating lipid metabolism, stearoyl-CoA desaturase activity modulates cell proliferation and survival and emphasize the important role of endogenously synthesized monounsaturated fatty acids in sustaining the neoplastic phenotype of transformed cells.
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Inhibition of Stearoyl-CoA Desaturase 1 expression in human lung adenocarcinoma cells impairs tumorigenesis.

TL;DR: This study demonstrates thatSCD1 activity regulates Akt activation and determines the rate of cell proliferation, survival and invasiveness in A549 cancer cells and shows, for the first time, that SCD1 is a key factor in the regulation of tumorigenesis in vivo.
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AKT1 and MYC Induce Distinctive Metabolic Fingerprints in Human Prostate Cancer

TL;DR: Findings show how prostate tumors undergo a metabolic reprogramming that reflects their molecular phenotypes, with implications for the development of metabolic diagnostics and targeted therapeutics.