% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Avenhaus:302113,
author = {A. Avenhaus$^*$ and B. Kuhn$^*$ and M. Velimirović$^*$ and
T. Strobel$^*$ and J. Bulkescher$^*$ and C. Lohrey$^*$ and
J. Krijgsveld$^*$ and F. Hoppe-Seyler$^*$ and K.
Hoppe-Seyler$^*$},
title = {{P}leiotropic {E}ffects of {M}etformin on the
{C}hemotherapy {R}esponse of {HPV}-{P}ositive {C}ancer
{C}ells.},
journal = {Journal of medical virology},
volume = {97},
number = {6},
issn = {0146-6615},
address = {Bognor Regis [u.a.]},
publisher = {Wiley},
reportid = {DKFZ-2025-01245},
pages = {e70434},
year = {2025},
note = {#EA:D365#LA:D365# Z999},
abstract = {Improved treatment strategies for HPV-positive cancers are
urgently required. The viral E6/E7 oncoproteins are
essential for the proliferation of HPV-positive cancer cells
and considered attractive therapeutic targets. Metformin is
proposed to be repurposed for cancer therapy, but this is
under controversial debate. We previously demonstrated that
E6/E7 expression and the proliferation of HPV-positive
cancer cells are repressed by Metformin. Here, we explore
the effects of Metformin on the phenotype of HPV-positive
cancer cells in detail, either applied as monotreatment or
in combination with chemotherapeutic agents. We provide
evidence that the downregulation of E6/E7 is not the primary
mechanism underlying Metformin's growth-inhibitory effect in
HPV-positive cancer cells. Specifically, compared to
targeted E6/E7 repression by RNA interference (RNAi),
Metformin treatment differently altered the expression of
growth regulatory proteins, exerted different effects on the
cell cycle, and was able to suppress growth even in the
presence of E6/E7. Furthermore, we found that cancer cells
pre-treated with Metformin become resistant to senescence
induction by the pro-senescent chemotherapeutic agent
Etoposide, likely as a secondary effect of Metformin-induced
growth inhibition. Finally, depending on experimental
conditions, we uncover divergent, even opposing, effects on
the proliferation of HPV-positive cancer cells when
Metformin is combined with Cisplatin, with p53 playing a key
role in these processes. Collectively, our results show that
Metformin exerts complex effects on the phenotype of
HPV-positive cancer cells, which are critically influenced
by experimental conditions. Our findings may also explain
the discrepant results in the literature, reporting
agonistic or antagonistic effects upon combining Metformin
with Cisplatin.},
keywords = {Metformin: pharmacology / Humans / Oncogene Proteins,
Viral: genetics / Oncogene Proteins, Viral: metabolism /
Cell Line, Tumor / Antineoplastic Agents: pharmacology /
Cell Proliferation: drug effects / Papillomavirus
Infections: virology / Papillomavirus E7 Proteins: genetics
/ Etoposide: pharmacology / Female / Metformin (Other) /
cervical cancer (Other) / chemotherapy (Other) / human
papillomavirus (HPV) (Other) / oncogenesis (Other) /
oncoproteins (Other) / Metformin (NLM Chemicals) / Oncogene
Proteins, Viral (NLM Chemicals) / Antineoplastic Agents (NLM
Chemicals) / Papillomavirus E7 Proteins (NLM Chemicals) /
Etoposide (NLM Chemicals)},
cin = {D365 / B230},
ddc = {610},
cid = {I:(DE-He78)D365-20160331 / I:(DE-He78)B230-20160331},
pnm = {314 - Immunologie und Krebs (POF4-314)},
pid = {G:(DE-HGF)POF4-314},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40522309},
pmc = {pmc:PMC12169209},
doi = {10.1002/jmv.70434},
url = {https://inrepo02.dkfz.de/record/302113},
}