Related Experiment Video

Updated: May 19, 2026

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry
11:39

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry

Published on: July 21, 2017

Apoptosis and autophagy have opposite roles on imatinib-induced K562 leukemia cell senescence

C Drullion1, C Trégoat, V Lagarde

  • 1Laboratoire hématopoïèse leucémique et cibles thérapeutiques, INSERM U1035, Université Bordeaux Ségalen, 33076 Bordeaux, cedex, France.

Cell Death & Disease
|August 18, 2012
PubMed

Insights

Imatinib therapy for chronic myeloid leukemia (CML) induces cell death via apoptosis and autophagy, but also triggers senescence. Apoptosis limits senescence, while autophagy appears to promote it.

Area of Science:

  • Oncology
  • Cell Biology
  • Pharmacology

Background:

  • Imatinib is a first-line therapy for chronic myeloid leukemia (CML).
  • Imatinib eliminates CML cells through apoptosis and autophagy.
  • The role of senescence in imatinib's mechanism of action is not fully understood.

Purpose of the Study:

  • To investigate the induction of senescence by imatinib in K562 CML cells.
  • To elucidate the interplay between apoptosis, autophagy, and senescence in response to imatinib.

Main Methods:

  • Analysis of imatinib-treated K562 cells for cell cycle arrest, p27 expression, and SA-β-Gal staining.
  • Modulation of apoptosis (caspase inhibition, Bim targeting, Bcl2 overexpression) and autophagy (ATG7, Beclin-1, ATG5 silencing).

Main Results:

  • Imatinib induces cell cycle arrest, p27 increase, and SA-β-Gal staining, indicative of senescence.
  • Inhibition of apoptosis potentiates imatinib-induced senescence.
  • Autophagy inhibition (ATG7, Beclin-1) reduces senescence, while ATG5 inhibition enhances it, suggesting a complex role.

Conclusions:

  • Imatinib induces senescence in CML cells, alongside apoptosis and autophagy.
  • Apoptosis acts as a limiting factor for imatinib-induced senescence.
  • Autophagy plays a complex, potentially opposing role in imatinib-induced senescence.

More Related Videos

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells12:44

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

Published on: October 11, 2012

Related Concept Videos

Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...