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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...
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PKCepsilon induces Bcl-2 by activating CREB.

Eswar Shankar1, Soumya Krishnamurthy, Rajiv Paranandi

  • 1Department of Molecular Biology and Immunology, University of North Texas Health Science Center and Institute for Cancer Research, Fort Worth, TX 76107, USA.

International Journal of Oncology
|March 4, 2010
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Protein kinase C epsilon (PKCepsilon) activates the transcription factor CREB to induce Bcl-2 expression in breast cancer cells. This PKCepsilon-CREB pathway regulates apoptosis and cell death, impacting cancer progression.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • Protein kinase C epsilon (PKCepsilon) is a known oncogene and anti-apoptotic protein.
  • Previous studies showed PKCepsilon overexpression in breast cancer cells reduces apoptosis.
  • The precise mechanism of Bcl-2 induction by PKCepsilon remained unclear.

Purpose of the Study:

  • To elucidate the mechanism by which PKCepsilon induces Bcl-2 expression in breast cancer cells.
  • To investigate the role of transcription factor CREB in PKCepsilon-mediated Bcl-2 regulation.

Main Methods:

  • Utilized siRNA to knockdown PKCepsilon, Akt, and CREB in MCF-7 and MDA-MB-231 breast cancer cell lines.
  • Assessed protein and mRNA levels of Bcl-2.
  • Measured phosphorylation of CREB at Ser133.
  • Evaluated sensitivity to TRAIL-mediated apoptosis.

Main Results:

  • PKCepsilon knockdown decreased Bcl-2 protein and mRNA levels in MDA-MB-231 cells.
  • PKCepsilon knockdown reduced CREB phosphorylation at Ser133 in MDA-MB-231 cells.
  • CREB depletion decreased Bcl-2 levels and sensitized cells to TRAIL-induced apoptosis.

Conclusions:

  • PKCepsilon regulates Bcl-2 induction through the activation of the transcription factor CREB.
  • The PKCepsilon-CREB pathway plays a critical role in regulating apoptosis in breast cancer cells.
  • Targeting this pathway could offer therapeutic strategies for breast cancer treatment.