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Microenvironmental IL1β promotes breast cancer metastatic colonisation in the bone via activation of Wnt signalling.
- Source :
-
Nature communications [Nat Commun] 2019 Nov 01; Vol. 10 (1), pp. 5016. Date of Electronic Publication: 2019 Nov 01. - Publication Year :
- 2019
-
Abstract
- Dissemination of tumour cells to the bone marrow is an early event in breast cancer, however cells may lie dormant for many years before bone metastases develop. Treatment for bone metastases is not curative, therefore new adjuvant therapies which prevent the colonisation of disseminated cells into metastatic lesions are required. There is evidence that cancer stem cells (CSCs) within breast tumours are capable of metastasis, but the mechanism by which these colonise bone is unknown. Here, we establish that bone marrow-derived IL1β stimulates breast cancer cell colonisation in the bone by inducing intracellular NFkB and CREB signalling in breast cancer cells, leading to autocrine Wnt signalling and CSC colony formation. Importantly, we show that inhibition of this pathway prevents both CSC colony formation in the bone environment, and bone metastasis. These findings establish that targeting IL1β-NFKB/CREB-Wnt signalling should be considered for adjuvant therapy to prevent breast cancer bone metastasis.
- Subjects :
- Animals
Antineoplastic Combined Chemotherapy Protocols pharmacology
Bone Neoplasms drug therapy
Bone Neoplasms secondary
Breast Neoplasms drug therapy
Breast Neoplasms pathology
Cell Line, Tumor
Female
HEK293 Cells
Humans
MCF-7 Cells
Mice, Inbred BALB C
Mice, Inbred NOD
Mice, Knockout
Mice, Nude
Mice, SCID
Neoplastic Stem Cells drug effects
Neoplastic Stem Cells pathology
Sulfasalazine administration & dosage
Tumor Microenvironment drug effects
Xenograft Model Antitumor Assays
Bone Neoplasms metabolism
Breast Neoplasms metabolism
Interleukin-1beta metabolism
Neoplastic Stem Cells metabolism
Wnt Signaling Pathway
Subjects
Details
- Language :
- English
- ISSN :
- 2041-1723
- Volume :
- 10
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Nature communications
- Publication Type :
- Academic Journal
- Accession number :
- 31676788
- Full Text :
- https://doi.org/10.1038/s41467-019-12807-0