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Interorgan communication in development and cancer

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Abstract Studies in model organisms have demonstrated that extensive communication occurs between distant organs both during development and in diseases such as cancer. Organs communicate with each other to coordinate growth and reach the correct size, while the fate of tumor cells depend on the outcome of their interaction with the immune system and peripheral tissues. In this review, we outline recent studies in Drosophila, which have enabled an improved understanding of the complex crosstalk between organs in the context of both organismal and tumor growth. We argue that Drosophila is a powerful model organism for studying these interactions, and these studies have the potential for improving our understanding of signaling pathways and candidate factors that mediate this conserved interorgan crosstalk. This article is categorized under: Establishment of Spatial and Temporal Patterns > Regulation of Size, Proportion, and Timing Early Embryonic Development > Development to the Basic Body Plan Invertebrate Organogenesis > Flies
Organ growth is coordinated with systemic body size control via interorgan crosstalk. The fat body (light brown) acts as a nutrient sensor and relays nutrient availability information to IPCs (orange) via secreted signals such as Upd‐2, GBPs, CCHamid2, Dawdle, ImpL2, Egr, and Sun, to regulate Ilps 2,3,5 secretion which activates systemic growth. Other mediators of fat body, muscle and wing discs are as depicted in the diagram, and explained in more details in the text. Fat body and brain crosstalk (inset). The fat body senses nutrient availability and sends a not yet identified signal to the glia cells (gray) in the brain. Glia cells produce Ilps 2,3,5, which trigger NSC (red) exit from quiescence and cell growth and division. Later in development, neurogenesis becomes nutrient‐independent and NSC proliferation relies on glia cell secretion of Jeb ligand. See text for more details
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Drosophila models of cancer‐associated cachexia: ImpL2 and Pvf1 induce systemic organ wasting in two different tumor types. ImpL2 and Pvf1 secreted by Yki‐overxpressing (green, left) or scrib, RasV12 (green, right) tumor cells are responsible for inducing wasting of muscle (pink), fat body (light brown) and ovaries (purple), by inducing insulin resistance and aberrant Pvr/MEK activation, respectively. See text for more details
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Polarity deficient tumors and immune system crosstalk. (a) Tumor suppressive interactions: Hemocytes (gray) are recruited to tumors caused by loss of cell polarity genes (scrib or dlg, green) and secrete Egr which activates JNK signaling in tumor cells. Several of the outputs of JNK activation, including the release of secreted factors such as Pvf1 and Upds, promote further hemocyte recruitment and proliferation as well as a systemic humoral response mediated by the fat body (light brown). See text for more details. These interactions with the immune system ultimately contribute to the elimination of tumor cells via apoptosis. (b) Tumor promoting interactions: In the presence of constitutive activation of the oncogene Ras, apoptosis in the polarity deficient cells (scrib, RasV12, green) is inhibited and the tumor suppressive function of the hemocytes (gray) is converted to tumor promoting. In this context, hemocyte‐secreted Egr promotes JNK‐mediated tumor proliferation and invasion. See text for more details
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Invertebrate Organogenesis > Flies
Early Embryonic Development > Development to the Basic Body Plan
Establishment of Spatial and Temporal Patterns > Regulation of Size, Proportion, and Timing