Related Experiment Video

Updated: May 4, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.1K

TGF-β promotes glioma cell growth via activating Nodal expression through Smad and ERK1/2 pathways

Jing Sun1, Su-zhi Liu2, Yan Lin1

  • 1Department of Neurology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.

Biochemical and Biophysical Research Communications
|December 28, 2013
PubMed

Insights

Transforming growth factor-beta (TGF-β) promotes glioma cell growth by increasing Nodal expression. This pathway, involving Smad3 and ERK1/2, offers a potential new therapeutic target for glioma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Transforming growth factor-beta (TGF-β) is known to influence glioma cell progression.
  • The precise molecular mechanisms by which TGF-β promotes glioma growth are still under investigation.

Purpose of the Study:

  • To elucidate a novel mechanism by which TGF-β enhances glioma cell proliferation.
  • To investigate the role of Nodal expression in TGF-β-mediated glioma cell growth.

Main Methods:

  • Glioma cells were treated with TGF-β, and Nodal expression was measured.
  • Smad2, Smad3, and ERK1/2 pathways were inhibited using siRNAs and pathway blockers.
  • Nodal expression was manipulated using Nodal-specific siRNA.
  • Cell proliferation, apoptosis, and invasion assays were performed.

Main Results:

  • TGF-β significantly upregulated Nodal expression in glioma cells.
  • TGF-β-induced Nodal expression was dependent on Smad3 and ERK1/2 signaling.
  • Nodal overexpression mimicked TGF-β's effects, promoting proliferation and invasion while inhibiting apoptosis.
  • Downregulating Nodal expression attenuated TGF-β's pro-growth effects and inhibited glioma growth independently.

Conclusions:

  • TGF-β promotes glioma cell growth primarily by enhancing Nodal expression.
  • The TGF-β/Nodal signaling axis represents a potential therapeutic target for glioma treatment.
Keywords:
ERK1/2Glioma cellNodalSmadTGF-β

More Related Videos

Translational Orthotopic Models of Glioblastoma Multiforme07:37

Translational Orthotopic Models of Glioblastoma Multiforme

Published on: February 17, 2023

3.7K
Spheroid Assay to Measure TGF-β-induced Invasion09:18

Spheroid Assay to Measure TGF-β-induced Invasion

Published on: November 16, 2011

20.8K

Related Concept Videos

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...
7.2K
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...
6.3K
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
64.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.6K
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...
2.9K