Related Experiment Video

Updated: May 30, 2026

Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics
12:28

Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics

Published on: January 11, 2019

Role of Apoptotic Proteins in REC-2006 Mediated Radiation Protection in Hepatoma Cell Lines

Pankaj Kumar Singh1, Raj Kumar, Ashok Sharma

  • 1Institute of Nuclear Medicine and Allied Sciences, Delhi, India.

Evidence-Based Complementary and Alternative Medicine : Ecam
|July 30, 2011
PubMed

Insights

REC-2006 enhances radiation protection in hepatoma cells by modulating apoptotic protein pathways. It inhibits key protein cleavage and cytochrome c release, offering greater protection in HepG2 cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Radiation Oncology

Background:

  • Hepatoma cell lines are susceptible to radiation-induced apoptosis.
  • Understanding the role of apoptotic proteins is crucial for developing radioprotective agents.

Purpose of the Study:

  • To evaluate the radioprotective role of REC-2006 in hepatoma cells.
  • To investigate the involvement of apoptotic proteins in REC-2006-mediated protection.

Main Methods:

  • Hepatoma cell lines (HepG2 and Hep3B) were treated with REC-2006 prior to irradiation.
  • Expression and cleavage of apoptotic proteins including ATM, PARP-1, AIF, cytochrome c, Apaf-1, caspase-9, caspase-3, ICAD, and CAD were analyzed.

Main Results:

  • REC-2006 inhibited cleavage of ATM and PARP-1, and reduced expression/translocation of AIF and cytochrome c in HepG2 cells.
  • REC-2006 significantly inhibited Apaf-1, caspase-9, and caspase-3 in HepG2 cells.
  • REC-2006 restored ICAD expression and lowered the nuclear to cytoplasmic CAD ratio in HepG2 cells, but not in Hep3B cells.

Conclusions:

  • REC-2006 provides significant radioprotection to HepG2 cells by modulating multiple apoptotic pathways.
  • REC-2006's protective mechanism involves inhibiting AIF translocation, ATM/PARP-1 cleavage, cytochrome c release, and caspase activation.
  • Differential effects of REC-2006 were observed between HepG2 and Hep3B cell lines, suggesting cell-specific responses.

More Related Videos

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry08:21

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry

Published on: September 1, 2019

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...
Cellular Injury V: Apoptosis and Autophagy01:22

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...
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.
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.