The SUMO System and TGFβ Signaling Interplay in Regulation of Epithelial-Mesenchymal Transition: Implications for Cancer Progression

被引:21
|
作者
Chanda, Ayan [1 ]
Sarkar, Anusi [1 ]
Bonni, Shirin [1 ]
机构
[1] Univ Calgary, Dept Biochem & Mol Biol, Arnie Charbonneau Canc Inst, Calgary, AB T2N 4N1, Canada
来源
CANCERS | 2018年 / 10卷 / 08期
基金
加拿大健康研究院; 加拿大自然科学与工程研究理事会;
关键词
SUMOylation; TGF beta; EMT; cancer; GROWTH-FACTOR-BETA; SMAD TRANSCRIPTIONAL ACTIVITY; E3 LIGASE ACTIVITY; UBIQUITIN LIGASE; TUMOR-SUPPRESSOR; E-CADHERIN; PROTEIN MODIFICATION; ACTIVATED STAT; BREAST-CANCER; STEM-CELLS;
D O I
10.3390/cancers10080264
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Protein post-translational modification by the small ubiquitin-like modifier (SUMO), or SUMOylation, can regulate the stability, subcellular localization or interactome of a protein substrate with key consequences for cellular processes including the Epithelial-Mesenchymal Transition (EMT). The secreted protein Transforming Growth Factor beta (TGF beta) is a potent inducer of EMT in development and homeostasis. Importantly, the ability of TGF beta to induce EMT has been implicated in promoting cancer invasion and metastasis, resistance to chemo/radio therapy, and maintenance of cancer stem cells. Interestingly, TGF beta-induced EMT and the SUMO system intersect with important implications for cancer formation and progression, and novel therapeutics identification.
引用
收藏
页数:20
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