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Breast cancer exploits neural signaling pathways for bone-to-meninges metastasis.
- Source :
-
Science (New York, N.Y.) [Science] 2024 Jun 21; Vol. 384 (6702), pp. eadh5548. Date of Electronic Publication: 2024 Jun 21. - Publication Year :
- 2024
-
Abstract
- The molecular mechanisms that regulate breast cancer cell (BCC) metastasis and proliferation within the leptomeninges (LM) are poorly understood, which limits the development of effective therapies. In this work, we show that BCCs in mice can invade the LM by abluminal migration along blood vessels that connect vertebral or calvarial bone marrow and meninges, bypassing the blood-brain barrier. This process is dependent on BCC engagement with vascular basement membrane laminin through expression of the neuronal pathfinding molecule integrin α6. Once in the LM, BCCs colocalize with perivascular meningeal macrophages and induce their expression of the prosurvival neurotrophin glial-derived neurotrophic factor (GDNF). Intrathecal GDNF blockade, macrophage-specific GDNF ablation, or deletion of the GDNF receptor neural cell adhesion molecule (NCAM) from BCCs inhibits breast cancer growth within the LM. These data suggest integrin α6 and the GDNF signaling axis as new therapeutic targets against breast cancer LM metastasis.
- Subjects :
- Animals
Female
Humans
Mice
Basement Membrane metabolism
Cell Line, Tumor
Cell Movement
Glial Cell Line-Derived Neurotrophic Factor genetics
Glial Cell Line-Derived Neurotrophic Factor metabolism
Laminin metabolism
Macrophages metabolism
Neoplasm Invasiveness
Neural Cell Adhesion Molecules metabolism
Neural Cell Adhesion Molecules genetics
Signal Transduction
Mice, SCID
Mice, Knockout
Bone Neoplasms secondary
Bone Neoplasms metabolism
Breast Neoplasms pathology
Breast Neoplasms metabolism
Breast Neoplasms genetics
Integrin alpha6 metabolism
Meningeal Neoplasms metabolism
Meningeal Neoplasms secondary
Meninges pathology
Neural Pathways metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1095-9203
- Volume :
- 384
- Issue :
- 6702
- Database :
- MEDLINE
- Journal :
- Science (New York, N.Y.)
- Publication Type :
- Academic Journal
- Accession number :
- 38900896
- Full Text :
- https://doi.org/10.1126/science.adh5548