Notch signals modulate lgl mediated tumorigenesis by the activation of JNK signaling
| Autor: | Mousumi Mutsuddi, Maimuna Sali Paul, Ankita Singh, D. Dutta, Ashim Mukherjee |
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| Rok vydání: | 2018 |
| Předmět: |
Cell death
0301 basic medicine SCRIB Notch genetic structures Carcinogenesis MAP Kinase Signaling System Notch signaling pathway lcsh:Medicine chemical and pharmacologic phenomena Context (language use) medicine.disease_cause lgl General Biochemistry Genetics and Molecular Biology 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Cell polarity medicine Animals Drosophila Proteins lcsh:Science (General) lcsh:QH301-705.5 Loss function JNK signaling Receptors Notch Chemistry Tumor Suppressor Proteins lcsh:R General Medicine Cell biology Research Note 030104 developmental biology lcsh:Biology (General) Tumor progression Models Animal Drosophila Tumor overgrowth 030217 neurology & neurosurgery lcsh:Q1-390 |
| Zdroj: | BMC Research Notes, Vol 11, Iss 1, Pp 1-9 (2018) BMC Research Notes |
| ISSN: | 1756-0500 |
| DOI: | 10.1186/s13104-018-3350-5 |
| Popis: | 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. 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. |
| Databáze: | OpenAIRE |
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