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Signaling interplay between transforming growth factor-β receptor and PI3K/AKT pathways in cancer

Long Zhang1, Fangfang Zhou, Peter ten Dijke

  • 1Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China; Department of Molecular Cell Biology, Cancer Genomics Centre and Centre for Biomedical Genetics, Leiden University Medical Center, Leiden, The Netherlands.

Trends in Biochemical Sciences
|November 19, 2013
PubMed

Insights

The transforming growth factor-beta (TGF-β) and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathways collaborate in cancer progression. Dual targeting of these signaling pathways offers a promising strategy for cancer treatment.

Area of Science:

  • Cellular Biology
  • Molecular Oncology
  • Cancer Signaling

Background:

  • Transforming growth factor-beta (TGF-β) exhibits dual roles in cancer, acting cytostatically in early stages and promoting oncogenesis in advanced cancers.
  • Phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling promotes cell survival and tumor formation.
  • Initially viewed as linear and potentially opposing, the TGF-β receptor and PI3K/AKT pathways are now understood to have complex interactions.

Purpose of the Study:

  • To explore the intricate crosstalk and collaborative signaling between the TGF-β and PI3K/AKT pathways.
  • To provide a rationale for investigating dual-targeting strategies in cancer therapy.

Main Methods:

  • Review and synthesis of existing literature on TGF-β and PI3K/AKT signaling.
  • Analysis of experimental evidence detailing pathway interactions and their roles in cancer.

Main Results:

  • Emerging evidence reveals complex signal integration and collaboration between TGF-β and PI3K/AKT pathways.
  • These pathways, once thought to counteract each other, actively cooperate in driving cancer progression.

Conclusions:

  • The intricate interplay between TGF-β and PI3K/AKT signaling is crucial for cancer development.
  • Targeting both pathways simultaneously presents a viable therapeutic approach for combating cancer.
Keywords:
AKTSMA- and MAD-related protein (SMAD) transforming growth factor-βmammalian target of rapamycin complexphosphatase and tensin homolog deleted on chromosome 10phosphoinositide 3-kinase

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