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@ARTICLE{Kong:285439,
author = {Y. Kong and Y. Liu and X. Li$^*$ and M. Rao and D. Li and
X. Ruan and S. Li and Z. Jiang and Q. Zhang},
title = {{P}almitoylation landscapes across human cancers reveal a
role of palmitoylation in tumorigenesis.},
journal = {Journal of translational medicine},
volume = {21},
number = {1},
issn = {1479-5876},
address = {London},
publisher = {BioMed Central},
reportid = {DKFZ-2023-02373},
pages = {826},
year = {2023},
note = {#EA:C070#},
abstract = {Protein palmitoylation, which is catalyzed by
palmitoyl-transferase and de-palmitoyl-transferase, plays a
crucial role in various biological processes. However, the
landscape and dynamics of protein palmitoylation in human
cancers are not well understood.We utilized 23
palmitoyl-acyltransferases and seven
de-palmitoyl-acyltransferases as palmitoylation-related
genes for protein palmitoylation analysis. Multiple publicly
available datasets were employed to conduct pan-cancer
analysis, examining the transcriptome, genomic alterations,
clinical outcomes, and correlation with c-Myc (Myc) for
palmitoylation-related genes. Real-time quantitative PCR and
immunoblotting were performed to assess the expression of
palmitoylation-related genes and global protein
palmitoylation levels in cancer cells treated with Myc
depletion or small molecule inhibitors. Protein docking and
drug sensitivity analyses were employed to predict small
molecules that target palmitoylation-related genes.We
identified associations between palmitoylation and cancer
subtype, stage, and patient survival. We discovered that
abnormal DNA methylation and oncogenic Myc-driven
transcriptional regulation synergistically contribute to the
dysregulation of palmitoylation-related genes. This
dysregulation of palmitoylation was closely correlated with
immune infiltration in the tumor microenvironment and the
response to immunotherapy. Importantly, dysregulated
palmitoylation was found to modulate canonical
cancer-related pathways, thus influencing tumorigenesis. To
support our findings, we performed a proof-of-concept
experiment showing that depletion of Myc led to reduced
expression of most palmitoylation-related genes, resulting
in decreased global protein palmitoylation levels. Through
mass spectrometry and enrichment analyses, we also
identified palmitoyl-acyltransferases ZDHHC7 and ZDHHC23 as
significant contributors to mTOR signaling, DNA repair, and
immune pathways, highlighting their potential roles in
tumorigenesis. Additionally, our study explored the
potential of three small molecular (BI-2531, etoposide, and
piperlongumine) to modulate palmitoylation by targeting the
expression or activity of palmitoylation-related genes or
enzymes.Overall, our findings underscore the critical role
of dysregulated palmitoylation in tumorigenesis and the
response to immunotherapy, mediated through classical
cancer-related pathways and immune cell infiltration.
Additionally, we propose that the aforementioned three small
molecule hold promise as potential therapeutics for
modulating palmitoylation, thereby offering novel avenues
for cancer therapy.},
keywords = {Cancer (Other) / DNA methylation (Other) / Immunotherapy
(Other) / Palmitoylation (Other) / Small molecular (Other) /
c-Myc (Other)},
cin = {C070},
ddc = {610},
cid = {I:(DE-He78)C070-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37978524},
pmc = {pmc:PMC10655258},
doi = {10.1186/s12967-023-04611-8},
url = {https://inrepo02.dkfz.de/record/285439},
}