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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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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...
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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Ibuprofen Induces Mitochondrial-Mediated Apoptosis Through Proteasomal Dysfunction.

Arun Upadhyay1, Ayeman Amanullah1, Deepak Chhangani1

  • 1Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan, India, 342011.

Molecular Neurobiology
|December 16, 2015
PubMed
Summary

Ibuprofen, a common nonsteroidal anti-inflammatory drug (NSAID), reduces proteasome activity and triggers apoptosis in cancer cells. Further research is needed to understand its anti-tumor mechanisms and potential in neurodegeneration.

Keywords:
AgeingApoptosisIbuprofenMitochondrial dysfunctionNSAIDsNeurodegenerationProteasome

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Area of Science:

  • Pharmacology
  • Molecular Biology
  • Oncology

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for their antipyretic, analgesic, and anti-inflammatory properties.
  • Emerging evidence suggests NSAIDs, including ibuprofen, may exert anti-proliferative effects on cancer cells by influencing apoptosis.
  • The precise molecular mechanisms by which NSAIDs induce apoptosis in cancer without adverse effects remain largely unelucidated.

Purpose of the Study:

  • To investigate the effects of ibuprofen on proteasome activity and apoptosis induction in cancer cells.
  • To explore the potential anti-tumor mechanisms of ibuprofen.
  • To assess the impact of ibuprofen on cellular processes relevant to cancer, neurodegeneration, and aging.

Main Methods:

  • Treatment of cancer cells with ibuprofen.
  • Assessment of proteasome activity and protein aggregation.
  • Analysis of mitochondrial function and cytochrome c release.

Main Results:

  • Ibuprofen treatment was observed to reduce proteasome activity.
  • Enhanced aggregation of ubiquitylated proteins and accumulation of proteasome substrates were noted.
  • Ibuprofen induced mitochondrial abnormalities and cytochrome c release into the cytosol.

Conclusions:

  • Ibuprofen impacts cellular mechanisms including proteasome function and mitochondrial integrity, leading to apoptosis.
  • These findings suggest ibuprofen has potential anti-tumor effects.
  • Further investigation into the molecular pathways of NSAIDs is warranted for therapeutic applications in cancer, neurodegeneration, and aging.