Autocrine LTA signaling drives NF-κB and JAK-STAT activity and myeloid gene expression in Hodgkin lymphoma.
Journal
Blood
ISSN: 1528-0020
Titre abrégé: Blood
Pays: United States
ID NLM: 7603509
Informations de publication
Date de publication:
28 03 2019
28 03 2019
Historique:
received:
22
08
2018
accepted:
22
01
2019
pubmed:
31
1
2019
medline:
4
12
2019
entrez:
31
1
2019
Statut:
ppublish
Résumé
Persistent NF-κB activation is a hallmark of the malignant Hodgkin/Reed-Sternberg (HRS) cells in classical Hodgkin lymphoma (cHL). Genomic lesions, Epstein-Barr virus infection, soluble factors, and tumor-microenvironment interactions contribute to this activation. Here, in an unbiased approach to identify the cHL cell-secreted key factors for NF-κB activation, we have dissected the secretome of cultured cHL cells by chromatography and subsequent mass spectrometry. We identified lymphotoxin-α (LTA) as the causative factor for autocrine and paracrine activation of canonical and noncanonical NF-κB in cHL cell lines. In addition to inducing NF-κB, LTA promotes JAK2/STAT6 signaling.
Identifiants
pubmed: 30696620
pii: S0006-4971(20)42671-0
doi: 10.1182/blood-2018-08-871293
doi:
Substances chimiques
Lymphotoxin-alpha
0
NF-kappa B
0
STAT6 Transcription Factor
0
STAT6 protein, human
0
JAK2 protein, human
EC 2.7.10.2
Janus Kinase 2
EC 2.7.10.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1489-1494Informations de copyright
© 2019 by The American Society of Hematology.