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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

11.8K

Transforming growth factor-β signaling: Tumorigenesis and targeting for cancer therapy

Amirhossein Ahmadi1, Masoud Najafi2, Bagher Farhood3

  • 1Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran.

Journal of Cellular Physiology
|December 12, 2018
PubMed

Insights

Transforming growth factor-beta (TGF-β) drives cancer progression and metastasis by influencing the tumor microenvironment. Targeting TGF-β signaling, particularly TβRII suppression, offers a promising therapeutic strategy for cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Aberrant expression of Transforming Growth Factor-beta (TGF-β) is linked to cancer progression and metastasis.
  • TGF-β, produced within the tumor microenvironment (TME), regulates cellular activity and promotes key cancer hallmarks.
  • TGF-β is a critical inducer of epithelial-mesenchymal transition (EMT), immune evasion, and metastasis.

Purpose of the Study:

  • To elucidate the multifaceted roles of TGF-β signaling in cancer.
  • To explore the canonical (Smad-dependent) and noncanonical (Smad-independent) pathways of TGF-β.
  • To review strategies for targeting TGF-β signaling in cancer therapy.

Main Methods:

  • Analysis of TGF-β's canonical (Smad-dependent) and noncanonical (Smad-independent) signaling pathways.
  • Examination of TGF-β's interactions with TβRI and TβRII receptors.
  • Review of non-Smad pathways involving MAPK, PI3K/Akt, and NF-κβ.

Main Results:

  • TGF-β signaling is complex, with pathway component deletions potentially yielding antitumor effects.
  • Tumor stage, type, and TGF-β concentration critically determine cancer progression or repression.
  • TGF-β signaling influences EMT, immune evasion, and metastasis through intricate molecular networks.

Conclusions:

  • TGF-β signaling is a pivotal regulator of cancer progression and metastasis.
  • Contextual factors, including tumor type and TGF-β concentration, modulate its role.
  • Targeting TGF-β receptors, specifically TβRII suppression, represents a key therapeutic avenue.
Keywords:
Smad4TβRIIcancer cellcancer stem cell (CSC)cancer therapyepithelial-mesenchymal transition (EMT)metastasistransforming growth factor (TGF)-βtumor microenvironment (TME)

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