Related Experiment Video

Updated: May 26, 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

Alterations in the Smad pathway in human cancers

Debangshu Samanta1, Pran K Datta

  • 1Departments of Cancer Biology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

Frontiers in Bioscience (Landmark Edition)
|December 29, 2011
PubMed

Insights

Transforming growth factor-beta (TGF-β) signaling impacts cancer, acting as a tumor suppressor but also aiding progression. Understanding its Smad-dependent pathway is key for developing novel cancer treatments.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Signaling

Background:

  • Members of the Transforming Growth Factor-beta (TGF-β) superfamily have diverse biological functions.
  • Aberrations in TGF-β signaling pathways are implicated in various clinical disorders, notably cancer.
  • TGF-β signaling can act as a tumor suppressor, evidenced by mutations in TGF-β receptors and Smads in human carcinomas.

Purpose of the Study:

  • To review recent advancements in understanding the Smad-dependent TGF-β pathway.
  • To explore the role of TGF-β signaling in human carcinogenesis.
  • To highlight the dual role of TGF-β in cancer progression and suppression.

Main Methods:

  • Literature review focusing on Smad-dependent TGF-β signaling.
  • Analysis of studies on TGF-β receptors and Smad proteins in cancer.
  • Examination of mouse models and human carcinoma data.

Main Results:

  • TGF-β signaling mutations are common in human carcinomas, supporting its tumor suppressor role.
  • TGF-β influences cell invasion, immune regulation, and the tumor microenvironment.
  • The outcome of TGF-β signaling is context-dependent, varying by tissue and cancer type.

Conclusions:

  • Understanding TGF-β superfamily signaling mechanisms is crucial for novel cancer therapy development.
  • The Smad-dependent pathway's role in carcinogenesis requires continued investigation.
  • Targeting TGF-β signaling offers potential therapeutic strategies for various cancers.

More Related Videos

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model09:00

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model

Published on: April 17, 2026

Live Cell Imaging of the TGF- β/Smad3 Signaling Pathway In Vitro and In Vivo Using an Adenovirus Reporter System11:06

Live Cell Imaging of the TGF- β/Smad3 Signaling Pathway In Vitro and In Vivo Using an Adenovirus Reporter System

Published on: July 30, 2018

Related Concept Videos

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...
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...
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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...