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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Emerging roles of Myc in stem cell biology and novel tumor therapies

Fig. 1

The molecular machinery underlying the maintenance of stemness in ES cells mainly regulated by c-Myc/Max complex. The transcriptional level of proto-oncogene c-Myc is promoted by leukemia inhibitory factor (LIF) and the transcriptional factor c-Myc forms a heterodimer with Max after phosphorylated by activated extracellular signal-regulated kinase (ERK). The c-Myc/Max complex suppresses GATA6 expression, and more importantly, forms the negative-feedback mechanism with the inhibition of phosphorylated ERK (p-ERK). Given that GATA6 and p-ERK induce apoptotic cell death of ES cells with caspase activation and reduce the degree of pluripotency of ES cells, the c-Myc/Max complex contributes to the viability and stemness of ES cells [3032]. Note that while red arrows indicate the activation/stimulation, blue ones show the inhibition/suppression

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