Related Experiment Video

Updated: Jun 26, 2026

Modeling the Early Steps of Ovarian Cancer Dissemination in an Organotypic Culture of the Human Peritoneal Cavity
09:00

Modeling the Early Steps of Ovarian Cancer Dissemination in an Organotypic Culture of the Human Peritoneal Cavity

Published on: December 31, 2015

The inhibitory effect of human embryonic germ cells on ovarian cancer

X Song1, B Kong, D Li

  • 1Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Ji'nan, Shandong, China.

Neoplasma
|January 20, 2009
PubMed

Insights

Human embryonic germ cells (hEGCs) significantly inhibit ovarian cancer SKOV3 cell growth. hEGCs induce apoptosis and downregulate AKT signaling, offering a potential new strategy for ovarian cancer treatment.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Stem Cell Biology

Background:

  • Cancer cells exhibit plasticity, sharing traits with pluripotent stem cells.
  • Tumor cell plasticity contributes to cancer development and progression.
  • Investigating interactions between stem cells and cancer cells offers therapeutic insights.

Purpose of the Study:

  • To investigate the effect of human embryonic germ cells (hEGCs) on SKOV3 ovarian cancer cells.
  • To determine if hEGCs can inhibit ovarian cancer cell growth and induce apoptosis.
  • To elucidate the molecular mechanisms underlying hEGC-mediated inhibition of SKOV3 cells.

Main Methods:

  • Coculturing SKOV3 cells with hEGCs.
  • Assessing apoptosis using TUNEL assay and caspase-9 activity via immunocytochemistry.
  • Quantifying AKT expression using real-time PCR and Western blot.
  • Evaluating hEGC efficacy in a SCID mouse xenograft model.

Main Results:

  • Coculture with hEGCs resulted in a 1.5-fold reduction in SKOV3 cell growth.
  • hEGCs induced apoptosis in SKOV3 cells, evidenced by caspase-9 activation.
  • AKT signaling pathway was downregulated in SKOV3 cells following hEGC treatment.
  • Tumor growth inhibition by hEGCs was confirmed in the in vivo animal model.

Conclusions:

  • hEGCs effectively inhibit the growth of SKOV3 ovarian cancer cells.
  • The inhibitory effect is mediated by the induction of apoptosis through caspase-9 activation.
  • Downregulation of the AKT pathway is a key mechanism in hEGC-induced tumor cell inhibition.
  • hEGCs represent a promising therapeutic agent for ovarian cancer.

More Related Videos

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

Assessment of Ovarian Cancer Spheroid Attachment and Invasion of Mesothelial Cells in Real Time14:25

Assessment of Ovarian Cancer Spheroid Attachment and Invasion of Mesothelial Cells in Real Time

Published on: May 20, 2014

Related Concept Videos

Oogenesis02:07

Oogenesis

In human women, oogenesis produces one mature egg cell or ovum for every precursor cell that enters meiosis. This process differs in two unique ways from the equivalent procedure of spermatogenesis in males. First, meiotic divisions during oogenesis are asymmetric, meaning that a large oocyte (containing most of the cytoplasm) and minor polar body are produced as a result of meiosis I, and again following meiosis II. Since only oocytes will go on to form embryos if fertilized, this unequal...
Nondisjunction01:21

Nondisjunction

Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold sister...
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...