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METAbolism of bone METAstasis (META2): Metabolic interactions between disseminated breast cancer cells and osteoblast lineage cells drive bone metastases formation

Project description

Metabolic link between early breast cancer bone metastases and osteoblasts

Triple-negative breast cancer (TNBC) cells metastasise to the bone, where they often stay dormant and remain undetectable for several years after initial colonisation. Recent studies showed that early-stage TNBC cells are in close proximity to osteoblasts (bone-forming cells), and this interaction promotes TNBC cell survival and proliferation. The objective of the EU-funded META2 project is to characterise the metabolism of TNBC cells in the bone and to prove that targeting this metabolism will prevent metastasis. The hypothesis is that to survive in the bone, TNBC cells rely on a nutrient requirements profile complementary to that of osteoblasts. A better understanding of the metabolism of TNBC cells in the bone is essential for the development of new diagnostics and therapeutic targets.

Objective

Triple negative breast cancer cells (TNBC) metastasize to the bone, resulting in progressive bone destruction and severe complications for the patient. TNBC colonize the bone already much earlier, but they often stay dormant for several years and remain undetectable. Recent studies showed that at this early stage, TNBC cells are in close proximity to bone-forming cells (osteoblasts), and this interaction promotes TNBC survival and proliferation. Interestingly, recent findings also indicate that the metabolism of tumor cells not only drives primary tumor growth, but also determines which cells will metastasize to lung or liver, indicating metabolic interactions of TNBC with their microenvironment. This concept may also apply to TNBC in bone, but insight in the metabolism of TNBC colonizing the bone is lacking. I hypothesize that to survive and thrive in the bone TNBC cells rely on a specific profile that is complementary in nutrient needs to osteoblasts. Accordingly, preliminary results of the lab showed that targeting glutamine pathway impaired bone metastasis formation. Thus, my objective is to characterize the metabolism of TNBC in bone at early time points and to validate that targeting this metabolism will limit or prevent bone metastasis. I will first perform metabolite dosage and transcriptomics on TNBC recovered at early stages of preclinical (mouse) models of bone metastasis. In parallel, I will decipher metabolic interactions in vitro between osteoblasts and TNBC using metabolomics. These two complimentary approaches will deliver fundamental insights into metabolic adaptations of TNBC during bone metastasis, and identification of the most interesting enzymes to target. I will then validate these targets through functional studies in preclinical models and analysis of expression levels in patient tumor samples. This better understanding of the metabolism of TNBC in the bone is essential for the development of new diagnostic tools and therapeutic targets.

Programme(s)

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Topic(s)

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Funding Scheme

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MSCA-IF-EF-ST - Standard EF

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Call for proposal

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(opens in new window) H2020-MSCA-IF-2018

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Coordinator

KATHOLIEKE UNIVERSITEIT LEUVEN
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 178 320,00
Address
OUDE MARKT 13
3000 LEUVEN
Belgium

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Region
Vlaams Gewest Prov. Vlaams-Brabant Arr. Leuven
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 178 320,00
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