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@ARTICLE{Scherr:285129,
author = {A.-L. Scherr and L. Nader and K. Xu and C. Elssner and D.
A. Ridder and F. Nichetti and M. Mastel$^*$ and S. Fritzsche
and E. Kelmendi and N. Schmitt and P. Hoffmeister-Wittmann
and S. M. E. Weiler and F. Korell$^*$ and T. Albrecht and M.
Schwab and H. Isele and A. Kessler and J. Hüllein and A.
Seretny$^*$ and L. Ye and T. Urbanik and S. Welte and A.-L.
Leblond and C. Heilig$^*$ and M. Rahbari$^*$ and A. Ali$^*$
and S. U. Gallage$^*$ and B. M. A. Lenoir$^*$ and N.
Wilhelm$^*$ and U. Gärtner and S. J. Ogrodnik$^*$ and C.
Springfeld and D. F. Tschaharganeh$^*$ and S. Fröhling$^*$
and T. Longerich and H. Schulze-Bergkamen and D. Jäger$^*$
and L. Brandl and P. Schirmacher and B. K. Straub and A.
Weber and E. N. De Toni and B. Goeppert and M.
Heikenwälder$^*$ and R.-F. Jackstadt$^*$ and S. Roessler
and K. Breuhahn and B. C. Köhler$^*$},
title = {{E}tiology-independent activation of the
{LT}β-{LT}β{R}-{RELB} axis drives aggressiveness and
predicts poor prognosis in {H}epatocellular carcinoma.},
journal = {Hepatology},
volume = {80},
number = {2},
issn = {0270-9139},
address = {[Alphen aan den Rijn]},
publisher = {Wolters Kluwer Health},
reportid = {DKFZ-2023-02253},
pages = {278-294},
year = {2024},
note = {2024 Aug 1;80(2):278-294 / DKFZ-ZMBH Alliance},
abstract = {Hepatocellular carcinoma (HCC) is the most common primary
liver tumor with an increasing incidence worldwide. HCC is a
heterogeneous malignancy and develops usually in a
chronically injured liver. The nuclear factor kappa B
(NF-κB) signaling network consists of a canonical and a
non-canonical branch. An activation of canonical NF-κB in
HCC is documented. However, a functional and clinically
relevant role of non-canonical NF-κB and its downstream
effectors is not established.Four human HCC cohorts (total
n=1,462) and four mouse HCC models were assessed for
expression and localization of NF-κB signaling components
and activating ligands. In vitro, NF-κB signaling,
proliferation and cell death were measured, proving a
pro-proliferative role of RELB activated via NIK. In vivo,
Lymphotoxin beta (LTβ) was identified as predominant
inducer of RELB activation. Importantly, hepatocyte-specific
RELB knockout in a murine HCC model led to a lower incidence
compared to controls and lower maximal tumor diameters. In
silico, RELB activity and RELB directed transcriptomics were
validated on the TCGA HCC cohort using inferred protein
activity and Gene Set Enrichment Analysis (GSEA). In
RELB-active HCC, pathways mediating proliferation were
significantly activated. In contrast to RELA, nuclear
enrichment of non-canonical RELB expression identified
patients with a poor prognosis in an etiology-independent
manner. Moreover, RELB activation was associated with
malignant features metastasis and recurrence.This study
demonstrates a prognostically relevant, etiology-independent
and cross-species consistent activation of a LTβ/LTβR/RELB
axis in hepatocarcinogenesis. These observations may harbor
broad implications for HCC, including possible clinical
exploitation.},
cin = {A013 / HD01 / F190 / B340 / F180 / D120 / B063},
ddc = {610},
cid = {I:(DE-He78)A013-20160331 / I:(DE-He78)HD01-20160331 /
I:(DE-He78)F190-20160331 / I:(DE-He78)B340-20160331 /
I:(DE-He78)F180-20160331 / I:(DE-He78)D120-20160331 /
I:(DE-He78)B063-20160331},
pnm = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
pid = {G:(DE-HGF)POF4-316},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37916976},
doi = {10.1097/HEP.0000000000000657},
url = {https://inrepo02.dkfz.de/record/285129},
}