Related Experiment Video

Updated: Jun 26, 2026

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice
10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

Myc down-regulation affects cyclin D1/cdk4 activity and induces apoptosis via Smac/Diablo pathway in an astrocytoma

D Amendola1, M De Salvo, R Marchese

  • 1Centro Ricerca S. Pietro, Fatebenefratelli Hospital, Rome, Italy.

Cell Proliferation
|January 16, 2009
PubMed
Abstract

Insights

Down-regulating Myc in astrocytoma cells inhibits proliferation and induces apoptosis. This suggests c-Myc is a potential therapeutic target for anticancer treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Astrocytomas are primary brain tumors with limited treatment options.
  • The c-Myc oncogene plays a critical role in cell proliferation and is often dysregulated in cancers.
  • Targeting c-Myc offers a potential strategy for novel anticancer therapies.

Purpose of the Study:

  • To investigate the antiproliferative effects of c-Myc down-regulation in human astrocytoma models.
  • To elucidate the mechanisms by which c-Myc inhibition affects cell cycle progression and induces apoptosis.

Main Methods:

  • Utilized inducible c-myc anti-sense RNA in T98G and ADF astrocytoma cell lines.
  • Assessed cell proliferation via trypan blue dye exclusion and cell cycle distribution by flow cytometry.
  • Analyzed cell cycle proteins using Western blot, co-immunoprecipitation, and RT-PCR.

Main Results:

  • Myc down-regulation caused G1 cell cycle arrest and S phase delay, inhibiting proliferation.
  • Inactive cyclin D1/cdk4 complexes were formed, with p57Kip2 and p27Kip1 contributing to inhibition.
  • Apoptosis was induced via the mitochondrial pathway, evidenced by cytochrome c and Smac/Diablo release and proteasome-mediated degradation of c-IAP.

Conclusions:

  • c-Myc down-regulation effectively inhibits astrocytoma cell proliferation and induces apoptosis.
  • The findings support c-Myc as a promising therapeutic target for astrocytoma treatment.
  • Further research into c-Myc-targeted therapies for brain tumors is warranted.

More Related Videos

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

Related Concept Videos

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...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...