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Federica Sotgia

Researcher at University of Salford

Publications -  250
Citations -  33056

Federica Sotgia is an academic researcher from University of Salford. The author has contributed to research in topics: Cancer cell & Stromal cell. The author has an hindex of 85, co-authored 247 publications receiving 28751 citations. Previous affiliations of Federica Sotgia include Manchester Academic Health Science Centre & The Breast Cancer Research Foundation.

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Cav1 suppresses tumor growth and metastasis in a murine model of cutaneous SCC through modulation of MAPK/AP-1 activation.

TL;DR: It is demonstrated that loss of Cav1 affects several characteristics associated with aggressive human skin tumors and that this protein may be an important modulator of tumor growth and invasion in cSCC.
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The reverse Warburg effect in osteosarcoma

TL;DR: The authors show that in this scenario, oxidative phosphorylation and ATP-production are increased in osteosarcoma cells by co-culture with MSCs, and that the ultimate effect is to increase the aggressive behavior of tumor cells, in particular their cell migration.
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17β-estradiol regulates giant vesicle formation via estrogen receptor-alpha in human breast cancer cells

TL;DR: The discovery of giant (3-42μm) intracellular and extracellular vesicles (GVs) and the role of E2 on vesicle formation in breast cancer (BC) cell lines using three independent live cell imaging techniques suggest that the GVs are regulated by E2 via ERα in ERα-positive BC but by E1-independent mechanisms in ER-ve BC.
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Mitochondrial markers predict survival and progression in non-small cell lung cancer (NSCLC) patients: Use as companion diagnostics.

TL;DR: It is concluded that mitochondrial biogenesis should be considered as a new therapeutic target, for the more effective treatment of human lung cancers.
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Mitoketoscins: Novel mitochondrial inhibitors for targeting ketone metabolism in cancer stem cells (CSCs)

TL;DR: This work concludes that OXCT1 and ACAT1 are important new therapeutic targets for further drug development and optimization and proposes that this new class of drugs should be termed “mitoketoscins”, to reflect that they were designed to target ketone re-utilization and mitochondrial function.