Related Experiment Video

Updated: Jun 22, 2026

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence
08:55

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence

Published on: November 2, 2014

Activin is a potent growth suppressor of epithelial ovarian cancer cells

Anassuya Ramachandran1, Elaine S Marshall, Donald R Love

  • 1Department of Obstetrics and Gynaecology, University of Auckland, Auckland, New Zealand. anassuya.ramachandran@medsci.ox.ac.uk

Cancer Letters
|June 5, 2009
PubMed

Insights

Activin, a major ovarian cytokine, inhibits proliferation in some epithelial ovarian cancer cell lines by inducing cell cycle arrest. Resistance is linked to reduced activin receptor expression, suggesting a re-evaluation of its role in ovarian cancer pathogenesis.

Area of Science:

  • Reproductive biology
  • Oncology
  • Cell signaling

Background:

  • Activin is a key ovarian cytokine with an undefined role in epithelial ovarian cancer (EOC).
  • Understanding activin's function in EOC is crucial for identifying new therapeutic targets.

Purpose of the Study:

  • To investigate the role of activin as a potential growth regulator in epithelial ovarian cancer.
  • To explore the mechanisms underlying activin's effect on EOC cell proliferation and identify potential resistance factors.

Main Methods:

  • Assessed the effect of activin on proliferation in 16 EOC cell lines.
  • Analyzed gene expression of activin receptors (ACTRIIA, ACTRIB) in responsive and unresponsive cell lines.
  • Investigated downstream signaling pathways, including SMAD2/3/4 activation, CDK inhibitor p15INK4B induction, C-MYC suppression, and cell cycle phase distribution (G1 arrest) in response to activin.

Main Results:

  • Activin demonstrated a growth inhibitory effect on 8 out of 16 EOC cell lines.
  • EOC cell lines unresponsive to activin exhibited downregulated expression of ACTRIIA and ACTRIB.
  • Responsive cell lines showed SMAD2/3/4 pathway activation, p15INK4B induction, C-MYC suppression, and G1 cell cycle arrest upon activin treatment.

Conclusions:

  • Activin acts as a potent inhibitor of proliferation in a subset of epithelial ovarian cancer cell lines.
  • Downregulation of activin receptors contributes to resistance against activin signaling in EOC.
  • The role of activin in epithelial ovarian cancer pathogenesis warrants further investigation and re-evaluation.

More Related Videos

An Ex Vivo Model of Ovarian Cancer Peritoneal Metastasis Using Human Omentum05:42

An Ex Vivo Model of Ovarian Cancer Peritoneal Metastasis Using Human Omentum

Published on: January 26, 2024

Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression12:42

Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression

Published on: August 28, 2012

Related Concept Videos

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...
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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...
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...