Modelling Cancer in Drosophila: The Next Generation


Drosophila melanogaster, the vinegar fly, has been utilised as a genetic amenable model organism for more than 100 years. In recent years, its use in modelling human cancer has been greatly expanding. In this article, an update of the recent advances in Drosophila research towards understanding cancer development is provided. Genetic analysis in Drosophila has provided considerable insight into the mechanisms controlling tissue growth and cell invasion/metastasis during tumourigenesis, as well as the importance of stem cells in tissue regeneration and cancer, and how genes cooperate in tumourigenesis. Several evolutionarily conserved signalling pathways are emerging as playing key roles in many of these processes, including the Jun kinase, Notch, Wnt, Jak/Stat and the Hippo tissue growth control pathway. Drosophila has also been specifically utilised to model certain human cancers, by expression of the human versions of cancer‐causing genes, including multiple endocrine neoplasia type 2, glioblastoma and acute myeloid leukaemia. Finally, the use of Drosophila as a vehicle for anticancer drug discovery is beginning to make an important impact in combating human cancer.

Key Concepts:

  • Drosophila is a useful system for modelling human cancer due to the high conservation of critical cancer‐causing genes between humans and flies.

  • Many signalling pathways contribute to tissue growth; however, the Hippo growth control pathway is emerging as playing a major role.

  • The Jun kinase signalling pathway plays a context‐dependent role in invasion/metastasis.

  • Cell polarity and differentiation factors play important roles in controlling the behaviour of stem cells, which can be usurped in cancer.

  • Cell competition mechanisms are important in removing damaged cells, and the perturbation of this control contributes to tumourigenesis.

  • Cancer is a cooperative process and Drosophila research has revealed many cooperating oncogenes and tumour suppressors.

  • Drosophila provides a useful model system to investigate specific human cancers including multiple endocrine neoplasia type 2, glioblastoma and acute myeloid leukaemia.

  • Drosophila can be utilised to screen for anticancer drugs.

Keywords: Drosophila; cancer; cell polarity; proliferation; survival; differentiation; invasion/metastasis; cell competition; tumour microenvironment; chemical screening

Figure 1.

Induction of invasion/migration by Src or Ret activation or Sin3a reduction. When patches of cells in the larval wing epithelium express Src or Ret or Sin3a‐RNAi, cells round up and become basally extruded and migrate/invade away from the domain of expression. This process is JNK dependent and involves the expression of MMPs (JNK targets) to enable breakdown of the extracellular matrix and cell extrusion. Rho1 and signalling from the disrupted adherens junctions is also important in promoting cell invasion. See text for details.

Figure 2.

Cell competition and compensatory cell proliferation: Diagrams of epithelial tissues undergoing cell competition or compensatory cell proliferation. Mutant cells are shown in green and wild‐type cells are shown in white. Wild‐type cells affected by compensatory cell competition are shown in beige. X indicates dying cells. See text for details. (a) Classical cell competition: Cells with reduced levels of Myc are eliminated by cell autonomous apoptosis. The Flower‐lose isoform (red dots) is expressed on the surface of the loser cells, marking them for elimination when in contact with the surrounding cells that express the ubiquitous isoform of Flower (not shown). Similarly, the elimination of cells with upregulated Hippo signalling (or yki mutants) is due to decreased Myc levels. However, Myc independent mechanisms are involved in cell competition of cells with decreased ribosomal function, Jak/Stat or Wg signalling. (b) Supercompetitors: Cells with a growth and proliferative advantage, such as cells overexpressing Myc, Jak/Stat or with increased Wg signalling or decreased Hippo signalling, act as ‘supercompetitors’ and are able to elicit noncell autonomous apoptosis in neighbouring wild‐type cells. Supercompetition by downregulation of the Hippo pathway occurs via upregulation of Myc, whereas Stat and Wg signalling induce supercompetitive behaviour by unknown mechanisms. (c) Cell competition of cell polarity regulator mutants: Aberrant cells are recognised by their epithelial neighbours or haemocytes (grey) and the JNK ligand, Eiger (TNF), is secreted from these cells. Mutant cells are removed by JNK‐dependent apoptosis. Activation of JNK in wild‐type boundary cells and PVR, ELMO and Mbc signalling is required for the removal of the dying cells. Haemocytes play the predominant role in engulfment and removal of the dead cells. (d) Noncell autonomous overgrowth – undead cells: Dying cells can emit morphogens (e.g. Wg, Dpp and Hh) to promote proliferation of their epithelial neighbours (beige), thereby restoring tissue size. However, when effector caspases are blocked in the dying cells (by expression of P35), these signals are sustained leading to noncell autonomous overgrowth. (e) Noncell autonomous overgrowth induced by mutants affecting cell polarity where the mutant cells undergo apoptosis: The ectopic activation of Notch signalling in vps25 or tsg101 (ept) mutant cells or of JNK signalling in scrib mutant cells leads to the expression and secretion of the JAK/STAT ligand, Upd, which promotes noncell autonomous proliferation and overgrowth of surrounding tissue (beige). Downregulation of the Hippo pathway is also involved in inducing the proliferation of the wild‐type cells. (f) Noncell autonomous overgrowth induced by mitochondrial mutants expressing RasV12 without mutant cell death: Mitochondrial mutants with RasV12 lead to the upregulation of ROS, which induces JNK activation. JNK then leads to downregulation of the Hippo pathway leading to expression of the targets, Upd and Wg, which act via the Jak/Stat and Wg pathways, respectively, in surrounding wild‐type cells to induce overgrowth (beige).

Figure 3.

Cooperative tumourigenesis: Diagrams of epithelial tissue undergoing various types of cooperative tumourigenesis. Mutant tissue in green, wild‐type cells are shown in white and RasV12 surrounding tissue is shown in red. See text for details. (a) Intraclonal cooperation with cell polarity mutants and RasV12 – JNK activation in the neoplastic tumour cells cooperates with activated Ras signalling to promote tumour overgrowth and invasion. (b) Interclonal cooperation with cell polarity mutants and RasV12 – cooperation occurs via induction of Upd from the scrib mutant cells (see Figure e), which induces upregulation of Jak/Stat signalling in the RasV12 cells to induce neoplastic overgrowth and invasion. (c) Interclonal cooperation with a mitochondrial mutant and RasV12 – cooperation occurs via induction of Upd and Wg from the mitochondrial mutant+RasV12 cells (see Figure f), which induce upregulation of Jak/Stat and Wg signalling, respectively, in the RasV12 cells to induce neoplastic overgrowth and invasion.



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Further Reading

Baena‐Lopez LA, Nojima H and Vincent JP (2012) Integration of morphogen signalling within the growth regulatory network. Current Opinion in Cell Biology 24(2): 166–172.

Boggiano JC and Fehon RG (2012) Growth control by committee: intercellular junctions, cell polarity, and the cytoskeleton regulate Hippo signalling. Developmental Cell 22(4): 695–702.

Das T and Cagan R (2010) Drosophila as a novel therapeutic discovery tool for thyroid cancer. Thyroid 20(7): 689–695.

Genevet A and Tapon N (2011) The Hippo pathway and apico‐basal cell polarity. Biochemical Journal 436(2): 213–224.

Gladstone M and Su TT (2011) Chemical genetics and drug screening in Drosophila cancer models. Journal of Genetics and Genomics 38(10): 497–504.

Kasai Y and Cagan R (2010) Drosophila as a tool for personalized medicine: a primer. Per Med 7(6): 621–632.

Lesage B, Gutierrez I, Martí E and Gonzalez C (2010) Neural stem cells: the need for a proper orientation. Current Opinion in Genetics and Development 20(4): 438–442.

Miles WO, Dyson NJ and Walker JA (2011) Modeling tumor invasion and metastasis in Drosophila. Disease Models and Mechanisms 4(6): 753–761.

Polesello C, Roch F, Gobert V, Haenlin M and Waltzer L (2011) Modelling cancers in Drosophila. Progress in Molecular Biology and Translational Science 100: 51–82.

Read RD (2011) Drosophila melanogaster as a model system for human brain cancers. Glia 59(9): 1364–1376.

Rudrapatna VA, Cagan RL and Das TK (2012) Drosophila cancer models. Developmental Dynamics 241(1): 107–118.

Tamori Y and Deng WM (2011) Cell competition and its implications for development and cancer. Journal of Genetics and Genomics 38(10): 483–495.

Worley MI, Setiawan L and Hariharan IK (2012) Regeneration and transdetermination in Drosophila imaginal discs. Annual Review of Genetics 46: 289–310.

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Cheng, Louise Y, Parsons, Linda M, and Richardson, Helena E(Mar 2013) Modelling Cancer in Drosophila: The Next Generation. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0020862.pub2]