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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.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
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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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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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The Intrinsic Apoptotic Pathway01:31

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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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mTOR Signaling and Cancer Progression03:03

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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.
The mTOR pathway or the...
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PI3K/mTOR/AKT Signaling Pathway01:22

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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Study of Protein-protein Interactions in Autophagy Research
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Inhibiting autophagy before it starts.

Yuqi Lin1, Biao Yu1,2, Pengfei Fang1,2

  • 1State Key Laboratory of Bioorganic and Natural Products Chemistry, Center for Excellence in Molecular Synthesis, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.

Autophagy
|April 10, 2023
PubMed
Summary
This summary is machine-generated.

Eltrombopag inhibits transcription factor EB (TFEB), blocking cancer cells

Keywords:
Autophagy inhibitionEltrombopagcancer therapyglioblastomathe transcription factor EB (TFEB)

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Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Drug Discovery

Background:

  • Autophagy is a cellular stress response exploited by cancer cells for growth and treatment resistance.
  • Targeting autophagy is a promising cancer therapy strategy, but effective clinical inhibitors are limited.
  • Existing research focuses on inhibiting autophagy-related enzymes like VPS34, ULK1, and ATG4B.

Purpose of the Study:

  • To identify novel autophagy inhibitors targeting transcriptional regulation.
  • To evaluate Eltrombopag's efficacy in inhibiting autophagy at the transcriptional level.
  • To assess Eltrombopag's potential in enhancing glioblastoma treatment.

Main Methods:

  • Discovery of Eltrombopag as a direct inhibitor of transcription factor EB (TFEB).
  • Investigation of Eltrombopag's mechanism in suppressing autophagic lysosomal gene expression.
  • Assessment of Eltrombopag combined with Temozolomide in glioblastoma models.

Main Results:

  • Eltrombopag inhibits TFEB, preventing the synthesis of autophagic lysosomal proteins.
  • This transcriptional inhibition effectively suppresses autophagy.
  • Eltrombopag enhances the therapeutic effect of Temozolomide against glioblastoma.

Conclusions:

  • Eltrombopag represents a novel class of autophagy inhibitors targeting transcriptional regulation.
  • Inhibiting TFEB offers a new strategy for cancer treatment.
  • Eltrombopag holds promise for improving glioblastoma therapy by overcoming treatment resistance.