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

被引：278

作者：

Zhang, Long ^{[1
,2
,3
]}

Zhou, Fangfang ^{[2
,3
]}

ten Dijke, Peter ^{[2
,3
,4
]}

机构：

[1] Zhejiang Univ, Inst Life Sci, Hangzhou 310058, Zhejiang, Peoples R China

[2] Leiden Univ, Med Ctr, Canc Genom Ctr, Dept Mol Cell Biol, Leiden, Netherlands

[3] Leiden Univ, Med Ctr, Ctr Biomed Genet, Leiden, Netherlands

[4] Uppsala Univ, Ludwig Inst Canc Res, Uppsala, Sweden

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2013年 / 38卷 / 12期

关键词：

AKT; phosphoinositide; 3-kinase; phosphatase and tensin homolog deleted on chromosome 10; SMA- and MAD-related protein (SMAD) transforming growth factor-beta; mammalian target of rapamycin complex; EPITHELIAL-MESENCHYMAL TRANSITION; NF-KAPPA-B; TGF-BETA; BREAST-CANCER; BONE METASTASIS; AKT; KINASE; SMAD; ACTIVATION; TRAF6;

D O I：

10.1016/j.tibs.2013.10.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The transforming growth factor (TGF)-beta and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathways are used in cells to control numerous responses, including proliferation, apoptosis, and migration. TGF-beta is known for its cytostatic effect's in premalignant states and its pro-oncogenic activity in advanced cancers. The pro-cell survival response exerted by growth-factor-mediated activation of PI3K/AKT has been linked to stimulation of tumor formation. Both TGF-beta receptor and PI3K/AKT pathways were initially modeled as linear signaling conduits. Although early studies suggested that these two pathways might counteract each other in balancing cell survival, emerging evidence has uncovered multiple modes of intricate signal integration and obligate collaboration in driving cancer progression. These new insights provide the rationale for exploring their dual targeting in cancer.

引用

页码：612 / 620

页数：9

共 75 条

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Activin/TGF-β induce apoptosis through Smad-dependent expression of the lipid phosphatase SHIP [J].