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4M8

Financiado

Formate-dependent Regulation of Cancer Metastasis

Mechanisms underlying cancer metastasis are poorly understood and context dependent. An essential feature of disseminating cancer cells is metabolic plasticity which allows cellular adaptation to changing environmental conditions... ver más

30/04/2029

LIH

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

LUXEMBOURG INSTITUTE OF HEALTH No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Ver 1 Participantes

Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2024-01-18

Línea de financiación objetivo El proyecto se financió a través de la siguiente ayuda:

ERC-2023-COG: ERC CONSOLIDATOR GRANTS

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Cerrada hace 1 año

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1 Participantes

LIH

2.00M€ | Lider

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Duración del proyecto: 63 meses Fecha Inicio: 2024-01-18
Fecha Fin: 2029-04-30

Líder del proyecto

LUXEMBOURG INSTITUTE OF HEALTH

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto Mechanisms underlying cancer metastasis are poorly understood and context dependent. An essential feature of disseminating cancer cells is metabolic plasticity which allows cellular adaptation to changing environmental conditions along the metastatic cascade. I discovered in 2016 the phenomenon of formate overflow, an alternative pathway for serine catabolism via folate-mediated one-carbon (1C) cycle. Instead of using formate for nucleotide synthesis (to support proliferation), formate overflow is characterised by formate excretion from cancer cells. Furthermore, I have convincingly demonstrated that mitochondrial 1C metabolism and increased extracellular formate concentrations promote cancer metastasis in a growth-independent manner. However, it remains unknown which intermediates of 1C metabolism contribute to this phenotype, how formate controls metastasis and how it can be targeted therapeutically. To cross the current edge of knowledge, I will (1) take advantage of genetic and newly developed analytical methods to dissect how the formate-dependent effects are propagated in cells; (2) describe intrinsic mechanisms to explain how the formate signal is relayed to promote metastasis and (3) exploit formate overflow for cancer cell killing by directly targeting the formate molecule. 4M8 will explain a novel concept of how a mitochondrial metabolic signal drives cancer cells towards a pro-metastatic phenotype and how this knowledge can be translated into a signature to analyse the metabolic state in human tumour samples. Finally, we will develop a novel tool to target formate directly within cancer cells. In sum, our research will shed light on an unexplored field of cancer metabolism providing the foundation to develop novel treatment approaches against metastatic cancer, the primary cause of cancer death.

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