Related Experiment Video

Updated: Aug 14, 2026

Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling
10:00

Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling

Published on: October 28, 2014

Short interfering RNA against the PDCD5 attenuates cell apoptosis and caspase-3 activity induced by Bax

L N Chen1, Y Wang, D L Ma

  • 1Laboratory of Medical Immunology, School of Basic Medical Science, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100083, People's Republic of China.

Apoptosis : an International Journal on Programmed Cell Death
|December 24, 2005
PubMed

Insights

Programmed cell death 5 (PDCD5) protein accelerates apoptosis. Inhibiting PDCD5 reduces apoptosis sensitivity and promotes cell proliferation, suggesting its role in cancer resistance.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Programmed cell death 5 (PDCD5) is crucial for apoptosis.
  • Reduced PDCD5 expression is observed in human carcinomas.
  • PDCD5's role in apoptosis regulation and cancer warrants further investigation.

Purpose of the Study:

  • To investigate the functional role of PDCD5 in apoptosis.
  • To determine the effect of PDCD5 suppression on apoptosis sensitivity and cell proliferation.
  • To elucidate the molecular mechanisms underlying PDCD5's function in apoptosis.

Main Methods:

  • Utilized short interfering RNA (siRNA) targeting PDCD5 (siPDCD5) to inhibit PDCD5 expression at mRNA and protein levels.
  • Assessed apoptosis sensitivity using Bax overexpression in HeLa, HEK293, and 293T cell lines.
  • Measured caspase-3 activity, procaspase-3 cleavage, cytochrome c release, and Bax translocation.
  • Performed MTT assays to evaluate cell proliferation.

Main Results:

  • siPDCD5 specifically inhibited PDCD5 expression.
  • Decreased PDCD5 expression reduced sensitivity to apoptosis induced by Bax overexpression.
  • siPDCD5 suppressed caspase-3 activity and procaspase-3 cleavage.
  • PDCD5 suppression attenuated cytochrome c release and Bax translocation to mitochondria.
  • Targeted PDCD5 suppression promoted cell proliferation.

Conclusions:

  • PDCD5 regulates apoptosis via the mitochondrial pathway, modulating Bax translocation, cytochrome c release, and caspase-3 activation.
  • Decreased PDCD5 expression may contribute to tumor cell resistance to apoptosis induced by anticancer drugs.
  • PDCD5 is a potential therapeutic target for overcoming cancer drug resistance.

More Related Videos

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation08:47

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

Related Concept Videos

Caspases01:24

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 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...
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...
Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...