Fluid shear stress regulates the survival of circulating tumor cells via nuclear expansion.
Level 5 - mechanism / opinion, no new human data
In vitro laboratory mechanobiology study without human clinical data.
PubMed 35510498 · doi:10.1242/jcs.259586
What was done
The authors exposed suspended circulating tumor cells (CTCs) and adherent tumor cells to fluid shear stress in vitro to assess cell viability, nuclear size, and histone acetylation. They also used pharmacological inhibition of histone acetylation to evaluate its role in shear-induced nuclear expansion and CTC apoptosis.
What was found
The abstract reports no numerical data or statistical measures. Qualitatively, fluid shear stress eliminated the majority of suspended CTCs and increased the nuclear size of surviving cells, while having no effect on adherent tumor cell viability and decreasing adherent cell nuclear size. Shear flow promoted histone acetylation in suspended tumor cells, and pharmacological inhibition of histone acetylation suppressed nuclear expansion and enhanced shear-induced apoptosis.
Why it matters
The findings describe a mechanotransduction mechanism whereby circulating tumor cells survive hemodynamic forces through epigenetic nuclear expansion. Targeting this survival mechanism could offer therapeutic strategies to eliminate metastatic tumor cells in circulation.
Limits
The abstract reports no quantitative values, sample sizes, specific tumor types, or cell lines. As an in vitro study, the findings do not capture the complexity of the in vivo circulatory environment, and clinical translation remains unverified.
Cited by
- supports Circulating tumor cells have mechanosensors on their surface and can undergo apoptosis in response to the mechanical shear stress and friction of blood flow during exercise.