Related Experiment Video
Updated: Jun 5, 2026

10:23
Evaluation of Caspase Activation to Assess Innate Immune Cell Death
Published on: January 20, 2023
Sage components enhance cell death through nuclear factor kappa-B signaling
Sally Joseph Deeb1, Chirine Omar El-Baba, Saadia Bashir Hassan
1Department of Biology, American University of Beirut, Beirut, Lebanon.
Frontiers in Bioscience (Elite Edition)
|January 4, 2011
Summary
Sage compounds linalyl acetate (Ly) and alpha-terpineol (Te) synergistically inhibit colon cancer cell growth by suppressing NF-kappaB signaling. This combination enhances apoptosis and potentiates chemotherapy, offering new therapeutic strategies.
Area of Science:
- Pharmacology
- Molecular Biology
- Oncology
Background:
- Sage compounds linalyl acetate (Ly) and alpha-terpineol (Te) show synergistic anti-proliferative effects.
- The NF-kappaB signaling pathway is a key regulator of cell proliferation, apoptosis, and inflammation in cancer.
Purpose of the Study:
- To investigate the effects of Ly and Te on NF-kappaB signaling in HCT-116 colon cancer cells.
- To explore the potential of Ly and Te as adjuncts to conventional chemotherapy.
Main Methods:
- Cell viability assays (MTT)
- Apoptosis and necrosis assays (PreG1)
- Electrophoretic mobility shift assays (EMSA) for NF-kappaB DNA binding
- Western blotting for p65 and IkappaB-alpha
- Gene expression analysis of NF-kappaB-regulated genes
Main Results:
- Ly and Te combinations reduced HCT-116 cell viability and induced apoptosis/necrosis.
- Combination treatment suppressed basal and TNF-alpha-induced NF-kappaB activation, inhibiting p65 nuclear translocation and IkappaB-alpha degradation via an IKK-independent mechanism.
- Ly and Te downregulated NF-kappaB-regulated antiapoptotic and proliferative genes.
- Combination treatment potentiated cell death induced by oxaliplatin and 5-FU.
Conclusions:
- Ly and Te anticancer activities are partly mediated through NF-kappaB suppression.
- These sage components can enhance apoptosis and potentiate chemotherapy, suggesting their potential in combination cancer therapy.
Related Concept Videos
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...
NF-κB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Overview of Cell Death
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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...
NF-kB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
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.
