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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Related Experiment Video

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Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
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Proteomic Analysis Reveals Trilaciclib-Induced Senescence.

Marina Hermosilla-Trespaderne1, Mark Xinchen Hu-Yang1, Abeer Dannoura2

  • 1Biosciences Institute, Newcastle University, Newcastle-upon-Tyne, UK; Faculty of Experimental Sciences, Universidad Francisco de Vitoria, Madrid, Spain.

Molecular & Cellular Proteomics : MCP
|April 28, 2024
PubMed
Summary

Trilaciclib, a CDK4/6 inhibitor, induces senescence in chronic myeloid leukemia cells, unlike cell death in other blood cancers. This suggests potential for hematological cancer therapy by halting cell cycle progression.

Keywords:
autophagyleukemiaproteomicssenescencetrilaciclib

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Induction and Validation of Cellular Senescence in Primary Human Cells
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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Trilaciclib is a cyclin-dependent kinase 4/6 inhibitor approved for myeloprotection in extensive-stage small cell lung cancer.
  • Its mechanism involves a temporary cell cycle halt in bone marrow cells.
  • The efficacy of trilaciclib in hematological cancers has not been previously explored.

Purpose of the Study:

  • To investigate the therapeutic potential of trilaciclib in hematological malignancies.
  • To understand the cellular effects of trilaciclib in chronic myeloid leukemia (CML).

Main Methods:

  • Mass spectrometry-based proteomics was employed to analyze molecular changes in K562 (CML) cells treated with trilaciclib.
  • Cellular responses, including cell cycle progression, proliferation, and cell death, were assessed.

Main Results:

  • Trilaciclib induced senescence in K562 cells, contrasting with cell death observed in acute myeloid leukemia, acute lymphoblastic leukemia, and myeloma cells.
  • In K562 cells, trilaciclib stabilized cyclin-dependent kinase 4/6, downregulated cell cycle proteins, and activated autophagy, inhibiting proliferation.
  • Senescence was also induced by trilaciclib in the nonsmall cell lung carcinoma cell line A549.

Conclusions:

  • Trilaciclib demonstrates potential as a therapeutic agent for hematological cancers.
  • Balancing senescence induction and autophagy modulation is crucial for trilaciclib treatment in CML and non-small cell lung cancer.