Related Experiment Video

Updated: Oct 23, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

p53-independent anisomycin induced G1 arrest and apoptosis in L1210 cell lines

A W He1, J G Cory

  • 1Department of Biochemistry, East Carolina University, School of Medicine, Greenville, NC 27858-4354, USA.

Anticancer Research
|May 5, 1999
PubMed

Insights

Protein synthesis inhibitors like anisomycin and cycloheximide affect cell cycle regulation. These compounds induce apoptosis in resistant L1210 cells (Y8) through a p53-independent pathway, impacting cell cycle arrest and Rb phosphorylation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • The L1210 cell line, when selected for resistance to deoxyadenosine (Y8), exhibits significantly reduced p53 mRNA and protein levels compared to wild-type (WT) L1210 cells.
  • Understanding the mechanisms of cell cycle regulation and apoptosis is crucial in cancer research.

Purpose of the Study:

  • To investigate the effects of protein synthesis inhibitors (anisomycin and cycloheximide) on WT and Y8 L1210 cells.
  • To determine if these effects are mediated by the p53 pathway.
  • To explore the role of cell cycle regulators like Rb and NF-kappa B.

Main Methods:

  • Treatment of WT and Y8 L1210 cells with anisomycin and cycloheximide.
  • Analysis of cell cycle arrest (G1 phase) and apoptosis induction.
  • Assessment of Rb phosphorylation and WAF1 protein levels.
  • Evaluation of NF-kappa B activation.
  • Investigation of caffeine's effect on cell cycle arrest.

Main Results:

  • Anisomycin and cycloheximide induced G1 arrest in WT cells and apoptosis in Y8 cells via a p53-independent mechanism.
  • A decrease in Rb phosphorylation was observed, but WAF1 protein was not induced.
  • Anisomycin activated NF-kappa B in WT cells but not in Y8 cells.
  • Cycloheximide was less potent than anisomycin in cell cycle arrest, apoptosis induction, and decreasing Rb phosphorylation.
  • Caffeine reversed the G1 arrest induced by these inhibitors in WT cells.

Conclusions:

  • The effects of anisomycin and cycloheximide on cell cycle regulation and apoptosis in L1210 cells are p53-independent.
  • These inhibitors likely act on cell cycle regulatory mechanisms rather than solely through protein synthesis inhibition.
  • NF-kappa B activation is involved in the response to anisomycin in WT cells.

More Related Videos

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method09:32

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Published on: September 10, 2017

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay13:10

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay

Published on: June 9, 2017

Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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...
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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...