TRAF4 mediates activation of TGF-β signaling and is a biomarker for oncogenesis in breast cancer
Fangfang Zhou, Fang Li, Feng Xie, ZhengKui Zhang, Huizhe Huang, Long Zhang
Abstract
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Fangfang Zhou, Fang Li, Feng Xie, ZhengKui Zhang, Huizhe Huang, Long Zhang
Abstract
Open-access reader
The tumor-promoting arm of transforming growth factor beta (TGF-β) receptor signaling contributes to advanced cancer progression and is considered a master regulator of breast cancer metastasis. In mammals, there are six distinct members in the tumor-necrosis factor receptor (TNFR)-associated factor (TRAF) family (TRAF1-TRAF6), with the function of TRAF4 not being extensively studied in the past decade. Although numerous studies have suggested that there is elevated TRAF4 expression in human cancer, it is still unknown in which oncogenic pathway TRAF4 is mainly implicated. This review highlights TGF-β-induced SMAD-dependent signaling and non-SMAD signaling as the major pathways regulated by TRAF4 involved in breast cancer metastasis.
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The tumor-promoting arm of transforming growth factor beta (TGF-β) receptor signaling contributes to advanced cancer progression and is considered a master regulator of breast cancer metastasis. In mammals, there are six distinct members in the tumor-necrosis factor receptor (TNFR)-associated factor (TRAF) family (TRAF1-TRAF6), with the function of TRAF4 not being extensively studied in the past decade. Although numerous studies have suggested that there is elevated TRAF4 expression in human cancer, it is still unknown in which oncogenic pathway TRAF4 is mainly implicated. This review highlights TGF-β-induced SMAD-dependent signaling and non-SMAD signaling as the major pathways regulated by TRAF4 involved in breast cancer metastasis.
Key concepts: SMAD, Cancer research, Transforming growth factor, Carcinogenesis, Signal transduction, Metastasis, Breast cancer, Transforming growth factor beta