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Fig. 6 | Molecular Cancer

Fig. 6

From: N-Myc promotes therapeutic resistance development of neuroendocrine prostate cancer by differentially regulating miR-421/ATM pathway

Fig. 6

A working model: N-Myc differentially regulating miR-421/ATM pathway contributes to ADT resistance and Enzalutamide resistance development of prostate cancer. N-Myc overexpression, if occurs in androgen-responsive stage (PCA cells), can overcome the ADT-induced senescence by downregulating ATM expression via miR-421 and promotes the outgrowth of ADT-resistant cancer cells. In contrast, N-Myc overexpression, if occurs in androgen-independent CRPC stage, up-regulates ATM expression by cooperating with EZH2 to suppress miR-421 expression and then de-repress its suppression on ATM. The N-Myc-induced upregulation of ATM contributes to the Enzalutamide resistance development and promotes the migration ability of CRPC cells

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Molecular Cancer

ISSN: 1476-4598