Related Experiment Video

Updated: Aug 7, 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

Transforming growth factor-beta1 and activin A generate antiproliferative signaling in thyroid cancer cells

Sílvia Emiko Matsuo1, Suzana Garcia Leoni, Alison Colquhoun

  • 1Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, Av Prof Lineu Prestes 1524, 05508-000 São Paulo, SP, Brazil.

The Journal of Endocrinology
|July 14, 2006
PubMed

Insights

Transforming growth factor-beta 1 (TGF-beta1) and activin A (ActA) both inhibit thyroid papillary carcinoma cell proliferation by regulating SMAD signaling. Gene silencing revealed their distinct roles in controlling cell growth and tumor development.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Endocrinology

Background:

  • Transforming growth factor-beta 1 (TGF-beta1) and activin A (ActA) signal through SMAD proteins.
  • TGF-beta1 inhibits thyroid follicular cell proliferation; ActA's role is less understood.
  • Both factors are co-expressed in thyroid tumors.

Purpose of the Study:

  • Investigate the specific roles of TGF-beta1 and ActA in thyroid papillary carcinoma cell proliferation and signaling.
  • Differentiate the contributions of TGF-beta1 and ActA using gene silencing.
  • Elucidate the regulation of SMAD proteins, SMAD7, and c-MYC by TGF-beta1 and ActA.

Main Methods:

  • Utilized TPC-1, a papillary thyroid carcinoma cell line.
  • Performed gene silencing of TGF-beta1 and ActA using RNA interference.
  • Analyzed mRNA expression of SMAD2, SMAD3, SMAD4, SMAD7, and c-MYC.
  • Assessed cell proliferation rates.
  • Administered recombinant TGF-beta1 and ActA.

Main Results:

  • Both TGF-beta1 and ActA knockdown led to increased TPC-1 cell proliferation.
  • Gene silencing reduced SMAD2, SMAD3, and SMAD4 mRNA expression.
  • Recombinant TGF-beta1 and ActA increased SMAD7 and decreased c-MYC expression.
  • Knockdown cells showed reduced SMAD7 and unexpectedly reduced c-MYC expression.
  • TGF-beta1 and ActA signaling pathways differentially regulate target genes.

Conclusions:

  • TGF-beta1 and ActA mediate SMAD signaling, impacting thyroid papillary carcinoma cell proliferation.
  • Both factors exhibit antiproliferative effects on thyroid cancer cells.
  • These findings highlight the potential roles of TGF-beta1 and ActA in thyroid tumorigenesis control.

More Related Videos

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

Spheroid Assay to Measure TGF-β-induced Invasion

Published on: November 16, 2011

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

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 are of three kinds RI, RII, and RIII. The RI...
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...
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...
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...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...