Related Experiment Video

Updated: Jun 20, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

Doxorubicin-mediated apoptosis in glioma cells requires NFAT3

Sreelatha Gopinath1, Sravan K Vanamala, Meena Gujrati

  • 1Department of Cancer Biology and Pharmacology, College of Medicine at Peoria, University of Illinois, 1649 Peoria, IL 61656, USA.

Cellular and Molecular Life Sciences : CMLS
|September 29, 2009
PubMed

Insights

Nuclear factor of activated T cells 3 (NFAT3) is crucial for doxorubicin-induced apoptosis in glioma cells. Inhibiting NFAT3 promotes cell survival and reverses the effects of doxorubicin on migration and invasion.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Nuclear factor of activated T cells (NFAT) transcription factors regulate critical cellular processes.
  • NFAT family members have been linked to various cancers.
  • The specific role of NFAT3 in glioma response to chemotherapy is not well understood.

Purpose of the Study:

  • To investigate the role of NFAT3 in doxorubicin (DOX)-induced apoptosis, migration, and invasion in SNB19 and U87 glioma cells.
  • To elucidate the molecular mechanisms by which NFAT3 influences chemoresistance and cell motility.

Main Methods:

  • Specific knockdown of NFAT3 using shNFAT3 (shNF3).
  • Doxorubicin (DOX) treatment of glioma cell lines.
  • Analysis of apoptosis-related proteins (TNF-alpha, TNFR1, caspase 10, caspase 3, PARP).
  • Assessment of cell migration and invasion using wound healing and matrigel assays.
  • Monitoring NFAT3 translocation to the nucleus via DOX treatment.

Main Results:

  • NFAT3 knockdown significantly inhibited doxorubicin-mediated apoptosis, promoting glioma cell survival.
  • Inhibition of NFAT3 downregulated key apoptotic markers including TNF-alpha, TNFR1, caspase 10, caspase 3, and PARP.
  • Doxorubicin treatment induced NFAT3 nuclear translocation.
  • NFAT3 inhibition reversed doxorubicin-induced suppression of cell migration and invasion.

Conclusions:

  • NFAT3 is essential for the induction of doxorubicin-mediated apoptosis in glioma cells.
  • NFAT3 plays a critical role in regulating chemoresistance, cell survival, migration, and invasion in response to doxorubicin.
  • Targeting NFAT3 may represent a novel therapeutic strategy for overcoming doxorubicin resistance in gliomas.

More Related Videos

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.