Related Experiment Video

Updated: Aug 24, 2026

Fluorescence-based Monitoring of PAD4 Activity via a Pro-fluorescence Substrate Analog
08:37

Fluorescence-based Monitoring of PAD4 Activity via a Pro-fluorescence Substrate Analog

Published on: November 5, 2014

Programmed cell death protein 4 (PDCD4) acts as a tumor suppressor in neuroendocrine tumor cells

Rüdiger Göke1, Cornelia Gregel, Alexandra Göke

  • 1Clinical Research Unit for Gastrointestinal Endocrinology, University of Marburg, Marburg, Germany. goeke@mailer.uni-marburg.de

Annals of the New York Academy of Sciences
|May 22, 2004
PubMed

Insights

Programmed cell death 4 (PDCD4) inhibits carcinoid cell proliferation by downregulating carbonic anhydrase II. This tumor suppressor gene

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Programmed cell death 4 (PDCD4) is recognized as a novel tumor suppressor.
  • Carcinoid tumors are a type of neuroendocrine tumor.
  • Cell proliferation is a critical factor in tumor growth.

Purpose of the Study:

  • To investigate the role of PDCD4 in regulating carcinoid cell proliferation.
  • To elucidate the molecular mechanisms underlying PDCD4's tumor suppressive function in carcinoid cells.

Main Methods:

  • Overexpression of PDCD4 in cultured carcinoid cells.
  • Assessment of cell proliferation rates.
  • Measurement of carbonic anhydrase type II (CA-II) expression levels.

Main Results:

  • Overexpression of PDCD4 significantly inhibited carcinoid cell proliferation.
  • PDCD4 overexpression led to a downregulation of CA-II.
  • Carbonic anhydrase II is implicated in bicarbonate production essential for cellular pathways.

Conclusions:

  • PDCD4 functions as a tumor suppressor in carcinoid cells.
  • PDCD4 inhibits proliferation potentially through the downregulation of carbonic anhydrase II.
  • Targeting the PDCD4-CA-II pathway may offer therapeutic strategies for carcinoid tumors.

More Related Videos

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

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...
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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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.