Publications by authors named "A Djiane"

The fat body in Drosophila larvae functions as a reserve tissue and participates in the regulation of organismal growth and homeostasis through its endocrine activity. To better understand its role in growth coordination, we induced fat body atrophy by knocking down several key enzymes of the glycolytic pathway in adipose cells. Our results show that impairing the last steps of glycolysis leads to a drastic drop in adipose cell size and lipid droplet content, and downregulation of the mTOR pathway and REPTOR transcriptional activity.

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The rising global incidence of cancer makes it the second leading cause of death worldwide. Over the past decades, significant progress has been made in both basic knowledge and the discovery of new therapeutic approaches. However, the complexity of mechanisms related to tumor development requires the use of sophisticated and adapted research tools.

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YAP and TAZ, the Hippo pathway terminal transcriptional activators, are frequently upregulated in cancers. In tumor cells, they have been mainly associated with increased tumorigenesis controlling different aspects from cell cycle regulation, stemness, or resistance to chemotherapies. In fewer cases, they have also been shown to oppose cancer progression, including by promoting cell death through the action of the p73/YAP transcriptional complex, in particular after chemotherapeutic drug exposure.

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Aggressive neoplastic growth can be initiated by a limited number of genetic alterations, such as the well-established cooperation between loss of cell architecture and hyperactive signaling pathways. However, our understanding of how these different alterations interact and influence each other remains very incomplete. Using Drosophila paradigms of imaginal wing disc epithelial growth, we have monitored the changes in Notch pathway activity according to the polarity status of cells (scrib mutant).

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Article Synopsis
  • Loss of the MAGI1 protein is linked to worse outcomes in luminal breast cancer and encourages tumor growth.
  • In MAGI1-deficient cells, the proteins E-cadherin and AMOTL2 accumulate, leading to increased stiffness and altered cellular signaling, including low YAP activity and high ROCK/p38 activity.
  • MAGI1 appears to act as a tumor suppressor by inhibiting the AMOTL2/p38 stress pathway, as blocking this pathway or removing AMOTL2 can reduce the tumor-promoting effects of MAGI1 loss.
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