RANKLed by the Complexity of Signaling in Breast Cancer Metastasis to the Brain.


Journal

Clinical breast cancer
ISSN: 1938-0666
Titre abrégé: Clin Breast Cancer
Pays: United States
ID NLM: 100898731

Informations de publication

Date de publication:
10 2020
Historique:
received: 19 01 2020
revised: 17 03 2020
accepted: 01 04 2020
pubmed: 10 5 2020
medline: 3 11 2021
entrez: 9 5 2020
Statut: ppublish

Résumé

Receptor activator of nuclear factor κB (RANK) and its ligand, RANKL, are essential for mammary gland development and play a vital role in breast carcinogenesis. RANKL-RANK signaling also drives thermoregulation and modulates inflammatory activation in the brain. The expression of RANKL in primary breast cancer (BC) has been negatively associated with brain metastases, while significantly higher levels of RANK are seen in BC with brain metastases. We examined the expression of RANK and RANKL in BC metastasis to the brain. We examined the expression of RANK and RANKL in 40 cases of BC metastasis to the brain. RANK was variably expressed in BC cells but minimally expressed in the adjacent brain parenchyma. In contrast, the expression of RANKL was minimal in metastatic BC but highly variable in tumoral stroma. RANKL expression in normal brain stroma obtained during autopsy was negligible. Histologic grade and BC subtypes were not significantly associated with RANK expression in metastatic BC. A significant negative correlation between RANK in metastatic BC and RANKL in tumoral stroma was identified (P < .001). RANK expressed by primary BC and RANKL detected in the tumor microenvironment together participate in cancer development, while the same principle may operate at distant sites. Further investigation is necessary to provide additional insight into the role of the RANKL-RANK pathway in BC progression and to investigate the potential efficacy of therapeutic strategies targeting these molecules in BC metastasis to the brain.

Sections du résumé

BACKGROUND
Receptor activator of nuclear factor κB (RANK) and its ligand, RANKL, are essential for mammary gland development and play a vital role in breast carcinogenesis. RANKL-RANK signaling also drives thermoregulation and modulates inflammatory activation in the brain. The expression of RANKL in primary breast cancer (BC) has been negatively associated with brain metastases, while significantly higher levels of RANK are seen in BC with brain metastases. We examined the expression of RANK and RANKL in BC metastasis to the brain.
PATIENTS AND METHODS
We examined the expression of RANK and RANKL in 40 cases of BC metastasis to the brain.
RESULTS
RANK was variably expressed in BC cells but minimally expressed in the adjacent brain parenchyma. In contrast, the expression of RANKL was minimal in metastatic BC but highly variable in tumoral stroma. RANKL expression in normal brain stroma obtained during autopsy was negligible. Histologic grade and BC subtypes were not significantly associated with RANK expression in metastatic BC. A significant negative correlation between RANK in metastatic BC and RANKL in tumoral stroma was identified (P < .001).
CONCLUSION
RANK expressed by primary BC and RANKL detected in the tumor microenvironment together participate in cancer development, while the same principle may operate at distant sites. Further investigation is necessary to provide additional insight into the role of the RANKL-RANK pathway in BC progression and to investigate the potential efficacy of therapeutic strategies targeting these molecules in BC metastasis to the brain.

Identifiants

pubmed: 32381383
pii: S1526-8209(20)30071-9
doi: 10.1016/j.clbc.2020.04.001
pii:
doi:

Substances chimiques

RANK Ligand 0
Receptor Activator of Nuclear Factor-kappa B 0
TNFRSF11A protein, human 0
TNFSF11 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e569-e575

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Kai Wang (K)

Department of Pathology, University of Alabama at Birmingham, Birmingham, AL.

James R Hackney (JR)

Department of Pathology, University of Alabama at Birmingham, Birmingham, AL.

Gene P Siegal (GP)

Department of Pathology, University of Alabama at Birmingham, Birmingham, AL.

Shi Wei (S)

Department of Pathology, University of Alabama at Birmingham, Birmingham, AL. Electronic address: swei@uabmc.edu.

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Classifications MeSH