Related Experiment Video

Updated: Dec 5, 2025

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells
06:32

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells

Published on: September 1, 2010

16.6K

VEGFC negatively regulates the growth and aggressiveness of medulloblastoma cells

Manon Penco-Campillo1, Yannick Comoglio1, Álvaro Javier Feliz Morel1

  • 1Université Côte d'Azur, Institute for Research on Cancer and Ageing of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Fédération Claude Lalanne (FCL), Nice, France.

Communications Biology
|October 17, 2020
PubMed

Insights

Vascular Endothelial Growth Factor C (VEGFC) surprisingly inhibits medulloblastoma (MB) cell aggressiveness and tumor growth. This finding challenges previous notions and suggests VEGFC as a potential therapeutic target for pediatric brain tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pediatric Neuro-oncology

Background:

  • Medulloblastoma (MB) is the most common pediatric brain tumor, with a 30% relapse rate within 5 years.
  • Metastatic dissemination in MB is linked to vascular endothelial growth factor C (VEGFC) and its receptors.
  • Current treatment strategies for MB have limitations, necessitating novel therapeutic targets.

Purpose of the Study:

  • To investigate the role of VEGFC in medulloblastoma cell aggressiveness and metastatic potential.
  • To determine if VEGFC acts as a positive or negative regulator of MB growth and dissemination.
  • To explore the VEGFC-dependent mechanisms underlying irradiation resistance in MB cells.

Main Methods:

  • Analysis of VEGFC expression correlation with MB cell proliferation and migration.
  • In vitro assessment of pseudo-vessel formation in MB cells.
  • Evaluation of VEGFC levels in irradiation-resistant MB cells.
  • Tumorigenicity assays in nude mice using MB cells with altered VEGFC expression.

Main Results:

  • VEGFC expression is inversely correlated with medulloblastoma cell aggressiveness, decreasing proliferation and migration.
  • Overexpression of VEGFC, observed in irradiation-resistant cells, impairs MB cell migration and pseudo-vessel formation.
  • MB cells overexpressing VEGFC or exhibiting irradiation resistance formed smaller tumors in vivo.
  • Irradiation reduces MB cell aggressiveness through a VEGFC-dependent pathway.

Conclusions:

  • VEGFC acts as a negative regulator of medulloblastoma growth and metastatic potential, contrary to established beliefs.
  • VEGFC-mediated inhibition of cell migration and proliferation offers a novel therapeutic avenue for MB.
  • Targeting VEGFC pathways may enhance treatment efficacy and reduce relapse rates in pediatric medulloblastoma.

More Related Videos

Intracranial Orthotopic Allografting of Medulloblastoma Cells in Immunocompromised Mice05:10

Intracranial Orthotopic Allografting of Medulloblastoma Cells in Immunocompromised Mice

Published on: October 3, 2010

12.5K
A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors09:04

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

Published on: March 15, 2016

10.0K

Related Concept Videos

Cells Coordinate Growth and Proliferation02:36

Cells Coordinate Growth and Proliferation

Cell size is a significant factor impacting cellular design, function, and fitness. There exists some internal coordination by which cells double their masses before division, thus, achieving homeostasis. Coordination between cell growth and proliferation depends on the checkpoints in between cell cycle phases. Loss of coordination or failure in the checkpoint mechanism can drive the cell to uncontrolled growth and loss of cellular function. Like dividing cells that coordinate cellular growth,...
4.9K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
7.5K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.6K
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
9.3K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
3.1K
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...
5.0K