Related Experiment Video

Updated: Jun 6, 2026

Analysis of Transforming Growth Factor ß Family Cleavage Products Secreted Into the Blastocoele of Xenopus laevis Embryos
06:57

Analysis of Transforming Growth Factor ß Family Cleavage Products Secreted Into the Blastocoele of Xenopus laevis Embryos

Published on: July 21, 2021

Bone morphogenetic protein 4 (BMP4) signaling in retinoblastoma cells

Maike Haubold1, Andreas Weise, Harald Stephan

  • 1Institute for Anatomy, Department of Neuroanatomy, University of Duisburg-Essen, Medical Faculty, 45122 Essen, Germany.

International Journal of Biological Sciences
|December 15, 2010
PubMed

Insights

Bone morphogenetic proteins (BMPs) induce apoptosis in retinoblastoma cells lacking the RB1 gene. However, BMP4 does not affect cell proliferation, indicating a failure in cell cycle control mechanisms.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Oncology

Background:

  • Bone morphogenetic proteins (BMPs) regulate cell proliferation and apoptosis in various tumors.
  • Retinoblastoma cells often lack a functional retinoblastoma (RB1) gene.
  • BMP receptors are present in retinoblastoma cell lines.

Purpose of the Study:

  • To investigate the role of the BMP4 pathway in retinoblastoma cells with absent RB1.
  • To understand how BMP4 signaling affects cell proliferation and apoptosis in these cells.

Main Methods:

  • Detection of BMP receptors in retinoblastoma cell lines.
  • Demonstration of BMP signaling via the Smad1/5/8 pathway in WERI-Rb1 cells.
  • Treatment of WERI-Rb1 cells with recombinant human BMP4.

Main Results:

  • BMP4 application increased apoptosis in WERI-Rb1 cells, largely independent of caspases.
  • BMP4 signaling did not affect cell proliferation despite the expression of pRb-related proteins.
  • Id proteins were significantly upregulated following BMP4 treatment.
  • No increase in p53, p21(CIP1), or p27(KIP1) expression was observed.

Conclusions:

  • BMP4 induces apoptosis in RB1-deficient retinoblastoma cells.
  • RB1 loss is not compensated by pRb-independent cell cycle control, preventing anti-proliferative responses to BMP4.
  • BMP4 signaling may offer a therapeutic target for retinoblastoma.
Keywords:
apoptosisbone morphogenetic proteincell cultureproliferationretinoblastoma

More Related Videos

Detection of Signaling Effector-Complexes Downstream of BMP4 Using in situ PLA, a Proximity Ligation Assay12:52

Detection of Signaling Effector-Complexes Downstream of BMP4 Using in situ PLA, a Proximity Ligation Assay

Published on: March 3, 2011

Reconstruct Human Retinoblastoma In Vitro06:52

Reconstruct Human Retinoblastoma In Vitro

Published on: October 11, 2022

Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
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.
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 hydroxylase and factor...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...