Related Experiment Video

Updated: Jul 18, 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 regulation of leukemia cells with the blockage of MDM2 by antisense oligonucleotides

Minghao Fang1, Xuemei Ji, Yi Tang

  • 1Department of Internal Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Journal of Huazhong University of Science and Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban
|November 24, 2006
PubMed

Insights

MDM2 specific antisense oligonucleotides inhibit MDM2 expression and increase P53 expression in leukemia cells. This approach enhances chemotherapy effectiveness by promoting apoptosis in HL60 cells.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • The MDM2-P53 pathway is a critical regulator of cell growth and apoptosis in cancer.
  • Targeting MDM2 offers a potential therapeutic strategy for leukemia.
  • Antisense oligonucleotides provide a method for specific gene silencing.

Purpose of the Study:

  • To investigate the effects of MDM2 specific antisense oligonucleotides on MDM2 and P53 expression in HL60 leukemia cells.
  • To evaluate the impact of MDM2 inhibition on apoptosis in combination with chemotherapy.

Main Methods:

  • Cell culture of HL60 leukemia cells.
  • Treatment groups: control, MDM2 antisense oligonucleotides (AS), cisplatin, and combined treatment.
  • Flow cytometry (FCM) analysis, Western blot, and RT-PCR to assess apoptosis and gene expression.

Main Results:

  • MDM2 specific antisense oligonucleotides significantly inhibited MDM2 expression (P < 0.01).
  • A significant increase in P53 expression was observed (P < 0.05).
  • Both MDM2 antisense oligonucleotides and cisplatin reduced the apoptosis rate (P < 0.01).

Conclusions:

  • MDM2 specific antisense oligonucleotides effectively inhibit MDM2 expression and induce P53 expression in leukemia cells.
  • This targeted inhibition enhances the apoptotic response of leukemia cells to chemotherapy.
  • MDM2 antisense oligonucleotides represent a promising therapeutic adjuvant for leukemia treatment.

More Related Videos

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype14:51

Pooled shRNA Library Screening to Identify Factors that Modulate a Drug Resistance Phenotype

Published on: June 17, 2022

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

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.
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...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
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...