Related Experiment Video

Updated: Aug 30, 2026

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation
09:09

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation

Published on: November 10, 2017

PTEN expression in PTEN-null leukaemic T cell lines leads to reduced proliferation via slowed cell cycle progression

Maria-Cristina Seminario1, Patricia Precht, Robert P Wersto

  • 1Laboratory of Cellular and Molecular Biology, National Institute on Aging, IRP/NIH/DHHS, Baltimore, MD 21224, USA.

Oncogene
|November 7, 2003
PubMed

Insights

The tumor suppressor PTEN reduces proliferation in leukaemic T cells by slowing cell cycle progression, not by inducing apoptosis. This occurs through PI3K signaling pathways, impacting cell growth and tumorigenesis.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • The balance between proto-oncogene phosphoinositide 3-kinase (PI3K) and tumor suppressor PTEN influences cellular growth, proliferation, and tumorigenesis.
  • Previous studies showed PTEN expression reduced proliferation in Jurkat T cell leukemia without cell cycle arrest.

Purpose of the Study:

  • To elucidate the mechanism by which PTEN expression inhibits proliferation in PTEN-null leukaemic T cells.
  • To investigate the role of cell cycle progression and apoptosis in PTEN-mediated antiproliferative effects.

Main Methods:

  • BrdU pulse-chase assays to track DNA synthesis and cell cycle progression.
  • Cell cycle arrest and release experiments.
  • Western blot analysis to assess protein levels of cyclins, CDKs, and apoptosis-related proteins.
  • Experiments involving active Akt and caspase inhibitors.

Main Results:

  • PTEN expression slowed cell cycle progression through all phases in leukaemic T cells.
  • This was accompanied by decreased levels of cyclins (A, B1, B2), cdk4, cdc25A, and increased p27KIP1.
  • Apoptosis was not a significant factor in PTEN's antiproliferative effect.
  • Active Akt blocked PTEN's antiproliferative effects, confirming PI3K pathway involvement.
  • Similar results were observed in the CEM T cell line.

Conclusions:

  • PTEN suppresses leukaemic T cell proliferation through an apoptosis-independent mechanism.
  • The primary mechanism involves delayed cell cycle transit, regulated by specific cell cycle proteins.
  • PTEN exerts its effects via conventional PI3K signaling pathways.

More Related Videos

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

Related Concept Videos

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...
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.
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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...
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...