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Fig. 7 | Cell Communication and Signaling

Fig. 7

From: IGFBP6 controls the expansion of chemoresistant glioblastoma through paracrine IGF2/IGF-1R signaling

Fig. 7

Model of paracrine-mediated regulation of chemoresistant cell proliferation in the context of glioma tumor heterogeneity. a TMZ-sensitive cells (blue) secrete IGFBP6, which binds and sequesters IGF2 produced by TMZ-resistant cells (red). As a consequence, IGF-1R and AKT signaling is not activated by IGF2, and proliferation of TMZ-resistant cells is suppressed. After TMZ treatment (b and c), the population of IGFBP6-producing, TMZ-sensitive cells is reduced, leaving extracellular IGF2 free and thus able to bind to and activate IGF-1R on the TMZ-resistant cells, thereby activating AKT signaling. Coordinate activation of IGF-1R and AKT enhances the proliferation of these chemoresistant glioma cells

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