Authors
Elvira Infante, Emmanuel Terriac, Matthieu Gelin, Vanessa Roca, Saline Jabre, Hugo Siegfried, David Pereira, Hugo Varet, Sara Khalilian, Atef Asnacios, Emma J van Bodegraven, Sandrine Etienne-Manneville
Published in
EMBO reports. Sep 04, 2026. Epub Sep 04, 2026.
Abstract
Vimentin intermediate filaments are a hallmark of aggressive tumours and are widely linked to invasion and EMT, yet how vimentin-dependent mechanics shape genome maintenance and therapy response is unclear. Here we show that vimentin, particularly under compressive load, promotes DNA repair competence. In contrast, vimentin-negative cells show impaired DNA damage sensing and downstream signaling, ultimately leading to decreased apoptosis and promoting cell survival under genotoxic stress at the expense of genomic stability. Using controlled cell compression together with genetic and pharmacological perturbations, we find that loss of vimentin in glioblastoma cells limits the expression and activity of core repair pathways because of induced nuclear mechanical compression. Relieving nuclear compression restores DNA damage accumulation and repair kinetics. Functionally, suppression of DNA damage responses enhances survival after clinically relevant DNA-damaging treatments, including temozolomide, X-Ray radiation and cell invasion through tight spaces. These findings invert the prevailing view that vimentin's contribution to tumour progression stems from enhanced migration and identify a mechanochemical vimentin-nucleus axis that tunes DNA damage responses to favor therapy tolerance and genome evolution.
PMID:
42698021
Bibliographic data and abstract were imported from PubMed on 05 Sep 2026.
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