Related Experiment Video

Updated: Aug 18, 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

Effects of transforming growth factor beta 1 on the growth of rhabdomyosarcoma cell line RD

Lü Ye1, Hong-ying Zhang, Hua Wang

  • 1Department of Pathology, West China Hospital, Sichuan University, Chengdu 610041, China.

Chinese Medical Journal
|May 19, 2005
PubMed
Abstract

Insights

Transforming growth factor-beta 1 (TGF-beta1) inhibits human rhabdomyosarcoma cell growth by inducing cell cycle arrest. This occurs via increased P27 protein, which suppresses CDK2 kinase activity, leading to G1-arrest.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Cancer Research

Background:

  • Transforming growth factor-beta (TGF-beta) is known to inhibit epithelial and endothelial cell growth.
  • The specific role of TGF-beta in regulating soft tissue sarcoma growth has been less explored.
  • This study investigates the effects of TGF-beta1 on human rhabdomyosarcoma (RD) cells.

Purpose of the Study:

  • To examine the impact of TGF-beta1 on the proliferation of human rhabdomyosarcoma (RD) cells.
  • To elucidate the underlying molecular mechanisms responsible for TGF-beta1's effects on RD cell growth.

Main Methods:

  • Cell viability assessed using [(3)H]-thymidine incorporation and MTT assays.
  • Cell cycle analysis performed via flow cytometry.
  • Protein and mRNA levels of cell cycle regulators detected by Western blot and RT-PCR; kinase activity assays and immunofluorescence used for further characterization.

Main Results:

  • TGF-beta1 significantly inhibited RD cell proliferation by inducing G1-arrest in the cell cycle.
  • TGF-beta1 prominently upregulated P27 expression, enhancing its binding to cyclinE-cdk2 complexes and suppressing cdk2 kinase activity.
  • P21 expression increased, c-myc decreased, while P15 and cdk4 were not implicated in the observed growth inhibition.

Conclusions:

  • TGF-beta1 effectively inhibits human rhabdomyosarcoma (RD) cell proliferation and induces G1-arrest.
  • The mechanism involves TGF-beta1-induced upregulation of P27, leading to the suppression of cdk2 kinase activity.
  • Upregulation of P21 and downregulation of c-myc may also contribute to the observed growth arrest.

More Related Videos

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

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...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
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...
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,...