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@ARTICLE{Zhou:300117,
author = {J. Zhou and M. He and Q. Zhao and E. Shi and H. Wang and V.
Ponkshe and J. Song and Z. Wu and D. Ji and G. Kranz and A.
Tscherne and S. Schwenk-Zieger and N. A. Razak and J. Hess
and C. Belka$^*$ and H. Zitzelsberger and I. Ourailidis and
F. Stögbauer and M. Boxberg$^*$ and J. Budczies and C. A.
Reichel and M. Canis and P. Baumeister and H. Wang and K.
Unger$^*$ and A. Mock and O. Gires},
title = {{EGFR}-mediated local invasiveness and response to
{C}etuximab in head and neck cancer.},
journal = {Molecular cancer},
volume = {24},
number = {1},
issn = {1476-4598},
address = {London},
publisher = {Biomed Central},
reportid = {DKFZ-2025-00615},
pages = {94},
year = {2025},
abstract = {Recurrent/metastatic head and neck squamous cell carcinoma
(R/M-HNSCC) is a severe, frequently lethal condition.
Oncogene addiction to epidermal growth factor receptor
(EGFR) is a hallmark of HNSCC, but the clinical efficacy of
EGFR-targeted therapies remains low. Understanding molecular
networks governing EGFR-driven progression is paramount to
the exploration of (co)-treatment targets and predictive
markers.We performed function-based mapping of
differentially expressed genes in EGFR-mediated local
invasion (fDEGs) using photoconvertible tracers and
RNA-sequencing (RNA-seq) in a cellular 3D-model.Upon
alignment with public single-cell RNA-seq (scRNA-seq)
datasets and HNSCC-specific regulons, a gene regulatory
network of local invasion (invGRN) was inferred from gene
expression data, which was overrepresented in budding
tumors. InvGRN comprises the central hubs inhibin subunit
beta alpha (INHBA) and snail family transcriptional
repressor 2 (SNAI2), and druggable fDEGs integrin subunit
beta 4 (ITGB4), laminin 5 (LAMB3/LAMC2), and sphingosine
kinase 1 (SPHK1). Blockade of INHBA repressed local invasion
and was reverted by activin A, laminin 5, and
sphingosine-1-phosphate, demonstrating a functional
interconnectivity of the invGRN. Epithelial-to-mesenchymal
transition (EMT) of malignant cells and the invGRN are
induced by newly defined EGFR-activity subtypes with
prognostic value that are promoted by amphiregulin (AREG)
and epiregulin (EREG). Importantly, co-inhibition of SPHK1
showed synthetic effects on Cetuximab-mediated invasion
blockade and high expression of selected fDEGs was
associated with response to Cetuximab in patient-derived
xenotransplantation (PDX) and R/M-HNSCC patients.We describe
an actionable network of EGFR-mediated local invasion and
define druggable effectors with predictive potential
regarding the response of R/M-HNSCC to Cetuximab.},
keywords = {Humans / ErbB Receptors: metabolism / ErbB Receptors:
genetics / Cetuximab: pharmacology / Cetuximab: therapeutic
use / Head and Neck Neoplasms: genetics / Head and Neck
Neoplasms: drug therapy / Head and Neck Neoplasms: pathology
/ Head and Neck Neoplasms: metabolism / Gene Expression
Regulation, Neoplastic: drug effects / Neoplasm Invasiveness
/ Cell Line, Tumor / Gene Regulatory Networks / Squamous
Cell Carcinoma of Head and Neck: genetics / Squamous Cell
Carcinoma of Head and Neck: drug therapy / Squamous Cell
Carcinoma of Head and Neck: pathology / Squamous Cell
Carcinoma of Head and Neck: metabolism / Animals /
Antineoplastic Agents, Immunological: therapeutic use /
Antineoplastic Agents, Immunological: pharmacology /
Cetuximab (Other) / EGFR (Other) / EMT (Other) / Invasive
gene regulatory network (Other) / Local invasion (Other) /
Oncogene addiction (Other) / R/M-HNSCC (Other) / fDEGs
(Other) / ErbB Receptors (NLM Chemicals) / Cetuximab (NLM
Chemicals) / EGFR protein, human (NLM Chemicals) /
Antineoplastic Agents, Immunological (NLM Chemicals)},
cin = {MU01},
ddc = {570},
cid = {I:(DE-He78)MU01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40121428},
doi = {10.1186/s12943-025-02290-1},
url = {https://inrepo02.dkfz.de/record/300117},
}