Hes1: a key role in stemness, metastasis and multidrug resistance.
Cancer Biol Ther
; 16(3): 353-9, 2015.
Article
en En
| MEDLINE
| ID: mdl-25781910
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.
Palabras clave
ABC, ATP-binding cassette; CSCs, cancer stem cells; CSL, CBF1/ Suppressor of Hairless / Lag1; EMT, epithelialmesenchymal transition; GSI, γ-secretase inhibitor; HDACs, histone deacetylases; Hes1; MAML, Mastermind-like protein family; MASH-1, Mammalian achaete-scute homolog-1; NICD, Notch intracellular domain; Notch signaling pathway; Runx2, Runt-related protein 2; TLE, transducin-like Enhancer of split; bHLH, basic helix-loop-helix; cancer stem cell; chemotherapy resistance; dnMAM, dominant-negative mastermind; metastasis; non-canonical Notch
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Células Madre Neoplásicas
/
Proteínas de Homeodominio
/
Resistencia a Antineoplásicos
/
Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico
/
Carcinogénesis
Límite:
Humans
Idioma:
En
Revista:
Cancer Biol Ther
Asunto de la revista:
NEOPLASIAS
/
TERAPEUTICA
Año:
2015
Tipo del documento:
Article
País de afiliación:
China