Related Experiment Video

Updated: Jun 2, 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

Inhibition of PRAME expression causes cell cycle arrest and apoptosis in leukemic cells

Norina Tanaka1, Yan-Hua Wang, Masayuki Shiseki

  • 1Department of Hematology, Tokyo Women's Medical University, Tokyo, Japan.

Leukemia Research
|May 10, 2011
PubMed

Insights

Preferentially expressed antigen of melanoma (PRAME) is crucial in acute leukemia progression. Knockdown of PRAME in leukemia cells suppressed proliferation and induced apoptosis, suggesting its role in disease advancement.

Area of Science:

  • Oncology
  • Molecular Biology
  • Hematology

Background:

  • Preferentially expressed antigen of melanoma (PRAME) is a known tumor-associated antigen.
  • The specific function of PRAME in leukemia pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the functional role of PRAME in acute leukemia.
  • To determine the correlation between PRAME expression and disease progression in leukemia patients.

Main Methods:

  • Small interfering RNA (siRNA)-mediated knockdown of PRAME in the K562 leukemia cell line.
  • Cell proliferation assays, cell cycle analysis, and apoptosis assays.
  • Analysis of PRAME expression levels and cell cycle S phase population in 32 acute leukemia patients at diagnosis and relapse.

Main Results:

  • PRAME knockdown in K562 cells led to suppressed proliferation, G(0)/G(1) cell cycle arrest, and induced apoptosis.
  • PRAME siRNA treatment altered gene expression related to erythroid differentiation.
  • Leukemia patients showed increased PRAME expression correlating with an elevated S phase population at relapse.

Conclusions:

  • PRAME plays a significant role in the proliferation and survival of leukemia cells.
  • PRAME expression is associated with disease progression in acute leukemia.
  • Targeting PRAME may represent a potential therapeutic strategy for acute leukemia.

More Related Videos

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia10:49

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia

Published on: September 18, 2013

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.
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...
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...
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...
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...