dMyc transforms cells into super-competitors.
By E. Moreno, Konrad Basler. Cell, 2004
598 citations recorded by the source corpus.
Overexpression of myc protooncogenes has been implicated in the genesis of many human tumors. Myc proteins seem to regulate diverse biological processes, but their role in tumorigenesis remains enigmatic. Here we use Drosophila imaginal discs to mimic situations in which cells with unequal levels of Myc protein are apposed and show that this invariably elicits a win/lose situation reminiscent of cell competition; cells with lower levels of dMyc are eliminated by apoptosis whereas cells with higher levels of dMyc over-proliferate. We find that this competitive behavior correlates with, and can be corrected by, the activation of the BMP/Dpp survival signaling pathway. Hence the heritable increase in dMyc levels causes cells to behave as "super-competitors" and reveals a novel mode of clonal expansion that causes, but also relies on, the killing of surrounding cells.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/c6498a4e625954279d71272a7fa4a9869f2797e9
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Citations in the corpus
- Growth arrest and autophagy are required for salivary gland cell degradation in Drosophila. (2007, unknown): “Cell death restricts tissue growth under conditions of cell competition during development (de la Cova et al., 2004; Moreno and Basler, 2004 ), but the influence that growth may have on the regulation of cell death remains unclear.”
- The influence of cell mechanics, cell-cell interactions, and proliferation on epithelial packing. (2007, background): “Furthermore, cells that differ from their neighbors in signaling capacity [22, 23], growth rate [24, 25], or cytoskeletal organization [26] are extruded from the epithelium, even when cell death is prevented.”