Hes1: a key role in stemness, metastasis and multidrug resistance

被引:153
作者
Liu, Zi-Hao [1 ]
Dai, Xiao-Meng [1 ]
Du, Bin [1 ]
机构
[1] Jinan Univ, Sch Med, Dept Pathol, Guangzhou, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
cancer stem cell; chemotherapy resistance; Hes1; metastasis; Notch signaling pathway; non-canonical Notch; CSCs; cancer stem cells; EMT; epithelial-mesenchymal transition; MASH-1; Mammalian achaete-scute homolog-1; bHLH; basic helix-loop-helix; TLE; transducin-like Enhancer of split; HDACs; histone deacetylases; dnMAM; dominant-negative mastermind; Runx2; Runt-related protein 2; ABC; ATP-binding cassette; NICD; Notch intracellular domain; CSL; CBF1; Suppressor of Hairless; Lag1; MAML; Mastermind-like protein family; GSI; -secretase inhibitor; NOTCH SIGNALING PATHWAY; SQUAMOUS-CELL CARCINOMA; PROSTATE-CANCER; BETA-CATENIN; OSTEOBLAST DIFFERENTIATION; TRANSCRIPTION REPRESSION; NEURONAL DIFFERENTIATION; OSTEOMIMETIC PROPERTIES; ENHANCES SENSITIVITY; PROGENITOR CELLS;
D O I
10.1080/15384047.2015.1016662
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Hes1 is one mammalian counterpart of the Hairy and Enhancer of split proteins that play a critical role in many physiological processes including cellular differentiation, cell cycle arrest, apoptosis and self-renewal ability. Recent studies have shown that Hes1 functions in the maintenance of cancer stem cells (CSCs), metastasis and antagonizing drug-induced apoptosis. Pathways that are involved in the up-regulation of Hes1 level canonically or non-canonically, such as the Hedgehog, Wnt and hypoxia pathways are frequently aberrant in cancer cells. Here, we summarize the recent data supporting the idea that Hes1 may have an important function in the maintenance of cancer stem cells self-renewal, cancer metastasis, and epithelial-mesenchymal transition (EMT) process induction, as well as chemotherapy resistance, and conclude with the possible mechanisms by which Hes1 functions have their effect, as well as their crosstalk with other carcinogenic signaling pathways.
引用
收藏
页码:353 / 359
页数:7
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