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Related Concept Videos

Autophagy01:27

Autophagy

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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.
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Delivery Pathways to the Lysosome01:36

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Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
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Autophagic Cell Death01:18

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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.
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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...
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Related Experiment Video

Updated: Jan 3, 2026

Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells
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Circumventing autophagy inhibition.

Christina G Towers1, Andrew Thorburn1

  • 1Department of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Cell Cycle (Georgetown, Tex.)
|November 19, 2019
PubMed
Summary
This summary is machine-generated.

Cancer cells can evade autophagy inhibition by upregulating NRF2 signaling, leading to resistance. Understanding these mechanisms is crucial for developing effective combination therapies to prevent tumor relapse.

Keywords:
ATG7AutophagyCRISPR/Cas9NRF2chloroquineproteasome

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Area of Science:

  • Oncology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Autophagy, a cellular recycling process, has a complex role in cancer, with preclinical studies suggesting a pro-tumorigenic function.
  • Numerous clinical trials are investigating autophagy inhibition combined with standard therapies for various cancer types.
  • Identifying cancer cell lines sensitive to autophagy gene loss is critical for therapeutic development.

Purpose of the Study:

  • To review recent publications on autophagy's role in cancer.
  • To explore mechanisms by which cancer cells circumvent autophagy inhibition.
  • To understand resistance to autophagy inhibition for improved clinical strategies.

Main Methods:

  • Utilized a novel, acute CRISPR/Cas9 assay to identify cancer cell lines sensitive to autophagy gene loss.
  • Analyzed rare cell populations that circumvented autophagy inhibition after initial sensitivity.
  • Investigated the role of NRF2 signaling in circumventing autophagy loss and maintaining protein homeostasis.

Main Results:

  • Identified cancer cell lines acutely sensitive to autophagy gene loss within 7 days.
  • Discovered rare clones that developed resistance to autophagy inhibition weeks later.
  • Found that circumventing cells upregulated NRF2 signaling, increasing sensitivity to proteasome inhibition and NRF2 knockdown.

Conclusions:

  • Cancer cells can develop resistance to autophagy inhibition through NRF2 pathway activation.
  • Understanding resistance mechanisms is key to preventing tumor relapse.
  • Preclinical studies can guide combination therapies to overcome autophagy inhibition resistance.