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Related Concept Videos

Drugs that Destabilize Microtubules01:10

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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 nucleolus is the most prominent substructure of the nucleus. When it was first discovered, it was considered to be an isolated organelle that forms fibrils and granules. In 1931, the relationship between the nucleolus and chromosomes was first described by Heitz. He observed that the appearance and size of nucleolus varies depending on the stage of the cell cycle. He also noticed constricted regions on different chromosomes clustered together at definite cell cycle stages. These regions,...
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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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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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Intermediate filaments (IFs) do not undergo spontaneous disassembly. Enzymes, kinases, and phosphatases add and remove phosphates from specific sites to regulate their disassembly. The IF concentration in the cytoplasm also regulates the disassembly. If the concentration crosses a threshold, it activates the protein kinases in the vicinity, allowing the phosphorylation of IFs.
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The destabilization of microtubules can occur during different stages of the microtubule lifecycle, such as nucleation or elongation. It can take place at either end of the microtubule or in the microtubule lattices as a whole. The lifespan of individual microtubules within a cell varies according to the cell type and stage of the cell cycle. During interphase, the lifespan of the microtubule is about 30 minutes, while during cell division, it is about 15 minutes. In axonal microtubules of...
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Related Experiment Video

Updated: Aug 22, 2025

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
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Oxaliplatin disrupts nucleolar function through biophysical disintegration.

H Broder Schmidt1, Zane A Jaafar1, B Erik Wulff1

  • 1Department of Biochemistry, Stanford University School of Medicine, Stanford, CA, USA.

Cell Reports
|November 9, 2022
PubMed
Summary
This summary is machine-generated.

Oxaliplatin, a colorectal cancer drug, disrupts nucleoli by causing liquid-liquid demixing. This leads to cell death by halting transcription and cell cycle progression.

Keywords:
CP: Cancercolorectal cancerdrug mechanismnucleolusphase separationtranscription/ translation inhibitors

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Platinum-based chemotherapy, including oxaliplatin, is crucial for cancer treatment.
  • The precise molecular mechanisms underlying platinum drug cytotoxicity and cancer specificity are not fully understood.

Purpose of the Study:

  • To elucidate the molecular basis of oxaliplatin's anti-cancer effects.
  • To investigate the impact of oxaliplatin on cellular structures and processes.

Main Methods:

  • Utilized biophysical techniques to observe nucleolar behavior.
  • Assessed cell-cycle progression and transcription.
  • Analyzed platinum compound partitioning within cells.

Main Results:

  • Oxaliplatin induces liquid-liquid demixing of nucleoli at therapeutic concentrations.
  • This disruption causes cell-cycle arrest and inhibits RNA Polymerase I-mediated transcription.
  • Data suggest oxaliplatin targets nucleolar RNA and proteins, not a single molecule.

Conclusions:

  • Oxaliplatin's cytotoxicity stems from inducing nucleolar phase separation, a biophysical defect.
  • This mechanism offers a novel strategy for targeting cellular processes within biomolecular condensates.
  • Understanding nucleolar function is key to developing new anti-cancer therapies.