Related Experiment Video

Updated: Jun 20, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Livin abrogates apoptosis of SPC-A1 cell by regulating JNKI signaling pathway

Yu-Sheng Chen1, Hong-Ru Li, Ming Lin

  • 1Department of Respiratory Medicine, Fujian Provincial Hospital, 350001, Fuzhou, Fujian, People's Republic of China. chenyushengfjsl@yahoo.com.cn

Molecular Biology Reports
|August 20, 2009
PubMed

Insights

Silencing livin, an apoptosis inhibitor, promotes cancer cell death. Livin may promote cancer cell survival by activating the JNK1 pathway and inhibiting caspase-3.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Livin, a novel inhibitor of apoptosis protein (IAP), is highly expressed in tumor tissues.
  • Livin is a potential therapeutic target in cancer treatment.
  • Silencing livin gene expression can promote tumor cell apoptosis and increase sensitivity to therapies.

Purpose of the Study:

  • To investigate the anti-apoptotic activity of livin.
  • To elucidate the molecular mechanisms underlying livin's effect on apoptosis.

Main Methods:

  • Gene silencing of livin.
  • Flow cytometry (FACS) analysis for cell apoptosis.
  • Western blotting to detect protein levels (cleaved caspase-3, total JNK1, phosphorylated JNK1).
  • Quantitative real-time PCR (qRT-PCR) to assess mRNA expression (caspase-3, JNK1).

Main Results:

  • Livin gene silencing significantly increased cancer cell apoptosis compared to controls (P < 0.05).
  • Knockdown of livin led to increased cleaved caspase-3 protein levels, while caspase-3 mRNA remained unchanged.
  • Phosphorylated JNK1 protein levels decreased after livin knockdown, with no significant changes in JNK1 mRNA or total JNK1 protein.

Conclusions:

  • Livin exerts anti-apoptotic effects on SPC-A1 cells.
  • Livin may function by activating the JNK1 signaling pathway.
  • Livin may inhibit caspase-3 activation, thereby promoting cell survival.

More Related Videos

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

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...
The Intrinsic Apoptotic Pathway01:31

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...
Apoptosis01:30

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 JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

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. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.