Related Experiment Video

Updated: Sep 25, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

[Effect of arsenic trioxide on the expression of cyclins gene in HL60 cells]

Jin-song Jia1, Shi-rong Xu, Jie Ma

  • 1Department of Hematology, Second Hospital, Hebei Medical University, Shijiazhuang 050000, China.

Zhonghua Nei Ke Za Zhi
|June 5, 2003
PubMed
Abstract

Insights

Arsenic trioxide treatment significantly alters gene expression in HL60 cells, inducing apoptosis. Key genes like Cyclin B1 and PCNA are implicated in this process.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Arsenic trioxide is a known chemotherapeutic agent.
  • Understanding its mechanism in leukemia cells is crucial.

Purpose of the Study:

  • Investigate gene expression changes in HL60 cells post-arsenic trioxide treatment.
  • Identify genes involved in arsenic trioxide-induced apoptosis.

Main Methods:

  • Gene expression profiling using gene chips.
  • Analysis of mRNA from treated and untreated HL60 cells.
  • Apoptosis detection via electron microscopy, DNA gel electrophoresis, and flow cytometry.

Main Results:

  • Arsenic trioxide altered the expression of 82 genes in HL60 cells (34 upregulated, 48 downregulated).
  • A concentration of 15 µmol/L arsenic trioxide induced significant apoptosis (26.1% vs 1.7% in control).

Conclusions:

  • Cyclin B1, proliferating cell nuclear antigen (PCNA), and insulin-like growth factor binding protein (IGFBP) are potentially key players in arsenic trioxide-induced HL60 cell apoptosis.

More Related Videos

Use of the Pyrimidine Analog, 5-Iodo-2′-Deoxyuridine (IdU) with Cell Cycle Markers to Establish Cell Cycle Phases in a Mass Cytometry Platform08:37

Use of the Pyrimidine Analog, 5-Iodo-2′-Deoxyuridine (IdU) with Cell Cycle Markers to Establish Cell Cycle Phases in a Mass Cytometry Platform

Published on: October 22, 2021

Related Concept Videos

Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
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...
Molecular Factors Affecting Cell Division01:27

Molecular Factors Affecting Cell Division

Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...