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Drugs that Stabilize Microtubules01:15

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Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
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Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
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The spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Updated: Jan 9, 2026

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
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Paclitaxel compromises nuclear integrity in interphase through SUN2-mediated cytoskeletal coupling.

Thomas Hale1, Victoria L Hale1, Piotr Kolata1

  • 1Structural Studies Division, MRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.

Journal of Cell Science
|December 10, 2025
PubMed
Summary
This summary is machine-generated.

Paclitaxel disrupts nuclear structure in interphase by affecting Lamin A/C (structural proteins) via the SUN2 protein. This nuclear disruption, alongside mitotic effects, contributes to paclitaxel

Keywords:
CancerLINCLamin A/CNucleusSUN2

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Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Biophysics

Background:

  • Lamin A/C is vital for nuclear integrity and mechanotransduction.
  • Altered Lamin A/C levels correlate with cancer prognosis and paclitaxel drug sensitivity.
  • Paclitaxel's anti-cancer effects extend beyond mitosis to poorly understood interphase mechanisms.

Purpose of the Study:

  • Investigate paclitaxel's interphase mechanism.
  • Elucidate the role of Lamin A/C and the LINC complex in paclitaxel's effects.
  • Determine the involvement of SUN2 in paclitaxel-induced nuclear changes.

Main Methods:

  • Advanced optical imaging and electron cryo-tomography.
  • Analysis of microtubule-vimentin bundle formation.
  • Assessment of Lamin A/C protein levels and nuclear organization.
  • Investigation of SUN2's role and regulation by polyubiquitination.

Main Results:

  • Paclitaxel induces nuclear aberrations in interphase via SUN2-dependent Lamin A/C disruption.
  • Aberrant microtubule-vimentin bundles form during paclitaxel treatment, causing nuclear deformation.
  • SUN2 is essential for paclitaxel-induced Lamin A/C reduction and is regulated by polyubiquitination.
  • Lamin A/C levels dictate cell survival and recovery post-paclitaxel treatment.

Conclusions:

  • Paclitaxel exerts anti-cancer effects through both mitotic disruption and interphase nuclear-cytoskeletal alterations.
  • SUN2-mediated Lamin A/C disruption is a key interphase mechanism of paclitaxel.
  • Understanding these mechanisms offers new insights into paclitaxel's efficacy and potential resistance.