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Comment
. 2015 Jul 11:17:92.
doi: 10.1186/s13058-015-0603-2.

Tipping the balance between good and evil: aberrant 14-3-3ζ expression drives oncogenic TGF-β signaling in metastatic breast cancers

Chevaun D Morrison  1 , William P Schiemann  2
Affiliations
Comment

Tipping the balance between good and evil: aberrant 14-3-3ζ expression drives oncogenic TGF-β signaling in metastatic breast cancers

Chevaun D Morrison et al. Breast Cancer Res. .

Abstract

Transforming growth factor beta (TGF-β) readily suppresses the development of early-stage breast cancers, an activity that gives way to tumor promotion in their late-stage counterparts. The molecular mechanisms underlying this mysterious switch in TGF-β function remain murky. In addressing this conundrum, Xu et al. observed aberrant 14-3-3ζ expression to prevent the formation of tumor-suppressive Smad2/3:p53 complexes, while simultaneously driving the generation of oncogenic Smad2/3:Gli2 complexes. Once formed, Smad2/3:Gli2 complexes stimulate the expression of parathyroid hormone-related protein necessary for breast cancer metastasis to bone. This viewpoint highlights 14-3-3ζ as an essential driver of oncogenic signaling by Smad2/3 and TGF-β in metastatic breast cancers.

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Figures

Fig. 1
Fig. 1
Tipping the balance in transforming growth factor beta (TGF-β) signaling in metastatic breast cancers. Expression of 14-3-3σ coordinates cytostatic TGF-β signals in premalignant MECs, while 14-3-3ζ expression and activity drives the acquisition of oncogenic TGF-β signaling in metastatic breast cancer cells. See text for additional details
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