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Fig. 3 | Molecular Cancer

Fig. 3

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

Fig. 3

N-Myc-induced down-regulation of ATM via miR-421 mediates the ADIS alleviation in LNCaP cells. a ATM inhibitor Ku60019 (10 μM) decreased ADT-induced senescence. Left panels showed representative images at indicated time points. Quantifications of SA-β-gal positively stained cells were indicated in the right panel. b RT-qPCR to show N-Myc overexpression increased miR-421 expression LNCaP cells but decreased miR-421 expression in C4–2 cells. c Immunoblots to show the decreased protein level of ATM in N-Myc overexpressing LNCaP cells but increased protein level of ATM in N-Myc overexpressing C4–2 cells. P84 is a loading control. d Transient transfection of miR-421 mimics leads to ATM suppression in both LNCaP and C4–2 cells. e Antisense morpholino oligonucleotide (AMO-miR421) increased the percentage of positive SA-β-gal staining cells in N-Myc overexpressed LNCaP cells upon ADT treatment. Upper panels showed representative images at day 4 and day 7. Quantifications of SA-β-gal positively stained cells were indicated in the lower panel. *p < 0.05; **p < 0.005

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