Notch signals modulate lgl mediated tumorigenesis by the activation of JNK signaling.
BMC Res Notes
; 11(1): 247, 2018 Apr 16.
Article
en En
| MEDLINE
| ID: mdl-29661224
ABSTRACT
OBJECTIVES:
Oncogenic potential of Notch signaling and its cooperation with other factors to affect proliferation are widely established. Notch exhibits a cooperative effect with loss of a cell polarity gene, scribble to induce neoplastic overgrowth. Oncogenic Ras also show cooperative effect with loss of cell polarity genes such as scribble (scrib), lethal giant larvae (lgl) and discs large to induce neoplastic overgrowth and invasion. Our study aims at assessing the cooperation of activated Notch with loss of function of lgl in tumor overgrowth, and the mode of JNK signaling activation in this context.RESULTS:
In the present study, we use Drosophila as an in vivo model to show the synergy between activated Notch (N act ) and loss of function of lgl (lgl-IR) in tumor progression. Coexpression of N act and lgl-IR results in massive tumor overgrowth and displays hallmarks of cancer, such as MMP1 upregulation and loss of epithelial integrity. We further show activation of JNK signaling and upregulation of its receptor, Grindelwald in N act /lgl-IR tumor. In contrast to previously described Notch act /scrib-/- tumor, our experiments in N act /lgl-IR tumor showed the presence of dying cells along with tumorous overgrowth.Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Muerte Celular
/
Sistema de Señalización de MAP Quinasas
/
Proteínas de Drosophila
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Proteínas Supresoras de Tumor
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Drosophila
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Receptores Notch
/
Carcinogénesis
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
BMC Res Notes
Año:
2018
Tipo del documento:
Article
País de afiliación:
India