Related Experiment Video

Updated: Aug 13, 2026

Spheroid Assay to Measure TGF-β-induced Invasion
09:18

Spheroid Assay to Measure TGF-β-induced Invasion

Published on: November 16, 2011

Effects of transforming growth factor beta-1 on growth-regulatory genes in tumour-derived human oral keratinocytes

I C Paterson1, V Patel, J R Sandy

  • 1Department of Oral and Dental Science, University of Bristol Dental Hospital and School, UK.

British Journal of Cancer
|October 1, 1995
PubMed

Insights

Transforming growth factor beta-1 (TGF-beta 1) impacts oral cancer cell growth by regulating c-myc and junB, independent of p53 mutations. TGF-beta 1

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Cancer Research

Background:

  • Transforming growth factor beta-1 (TGF-beta 1) is a key regulator of cell growth and differentiation.
  • Oral keratinocytes, both normal and carcinoma-derived, exhibit varying responses to TGF-beta 1.
  • Dysregulation of cell cycle proteins like c-myc, RB1, junB, and p53 is common in cancer.

Purpose of the Study:

  • To investigate the effects of TGF-beta 1 on c-myc, RB1, junB, and p53 expression and Rb protein phosphorylation in oral keratinocytes.
  • To determine if TGF-beta 1-induced growth inhibition is dependent on p53 status or Rb phosphorylation in oral cancer cells.

Main Methods:

  • Analysis of c-myc, RB1, junB, and p53 mRNA and protein expression in response to TGF-beta 1.
  • Assessment of pRb phosphorylation status in oral keratinocytes treated with TGF-beta 1.
  • Comparison of TGF-beta 1 responses in normal and carcinoma-derived oral keratinocytes.

Main Results:

  • c-myc amplification was observed in all tested tumor cell lines.
  • TGF-beta 1 down-regulated c-myc expression, correlating with growth inhibition, except in partially responsive tumor cells.
  • RB1 mRNA was unaffected, but underphosphorylated Rb protein accumulated in all cells.
  • junB expression was upregulated by TGF-beta 1 across different cell lines.
  • p53 mRNA and protein levels remained unchanged by TGF-beta 1 treatment in all cells, which harbored mutant p53.

Conclusions:

  • TGF-beta 1-mediated growth control can operate independently of mutant p53 and alterations in Rb phosphorylation or c-myc down-regulation.
  • Tumor cells can retain TGF-beta 1 sensitivity through alternative pathways even if one pathway is lost during cancer progression.
  • TGF-beta 1 likely employs multiple mechanisms for growth inhibition in oral keratinocytes.

More Related Videos

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates08:19

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates

Published on: April 22, 2019

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

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

Published on: October 27, 2020

Related Concept Videos

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...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
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...
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,...
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...