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Caspases

Caspases

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 cells.

The Intrinsic Apoptotic Pathway

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...

Apoptosis

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.

The Extrinsic Apoptotic Pathway

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...

Cellular Injury V: Apoptosis and Autophagy

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...

Autophagic Cell Death

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...

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Related Experiment Video

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Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Capsaicin induces apoptosis through ubiquitin-proteasome system dysfunction.

Ranjan Maity¹, Jaiprakash Sharma, Nihar Ranjan Jana

¹Cellular and Molecular Neuroscience Laboratory, National Brain Research Centre, Manesar, Gurgaon 122 050, Haryana, India.

Journal of Cellular Biochemistry

|January 14, 2010

Summary

Capsaicin, found in red pepper, induces cancer cell death by inhibiting proteasome function and triggering apoptosis. This research supports its potential as an anticancer drug.

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Area of Science:

Oncology
Molecular Biology
Pharmacology

Background:

Capsaicin, a red pepper component, exhibits antiproliferative effects on cancer cells.
Evidence suggests capsaicin induces apoptosis, but its molecular mechanisms are unclear.

Purpose of the Study:

To elucidate the molecular mechanisms of capsaicin-induced apoptosis.
To investigate the role of cellular proteasome function in capsaicin's anticancer effects.

Main Methods:

Treatment of mouse neuro 2a cells with capsaicin.
Assay of proteasome activity and protein levels (ubiquitinated proteins, p53, Bax, p27).
Analysis of apoptosis pathways, including the intrinsic mitochondrial pathway.

Main Results:

Capsaicin inhibits cellular proteasome function in a dose- and time-dependent manner, correlating with cell death.
Capsaicin induces oxidative stress, leading to the accumulation of ubiquitinated proteins and proteasome substrates.
Capsaicin triggers the intrinsic apoptosis pathway and promotes neurite outgrowth.

Conclusions:

Capsaicin-induced apoptosis is mediated by proteasome inhibition.
Capsaicin's mechanism involves oxidative stress and subsequent protein accumulation.
Results support capsaicin's potential as a novel anticancer therapeutic agent.