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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: The role of c-Myc-RBM38 loop in the growth suppression in breast cancer

Fig. 4

RBM38 destabilizes the c-Myc transcript by directly binding to c-Myc mRNA. a, b Ectopic expression of RBM38 shortened the half-life of c-Myc transcript. a MCF-7 (7) and b ZR-75-1 (ZR) cells were transfected with lentivirus to overexpress RBM38. The control (NC) and RBM38 overexpression (RBM38) cells were treated with 5 μg/ml actinomyclin D (Act D) for various times (0, 1, 2, 4, 6 h). Total RNAs were harvested, and then subjected to qRT-PCR analysis. c, d Knockdown of RBM38 lengthened the halflife of c-Myc transcript. c MCF-7 (7) and d ZR-75-1 (ZR) cells were transfected with the control (SCR) and RBM38 knockdown lentivirus (shRBM38). The following experiments were conducted as described in RBM38 overexpression. The relative quantification was calculated by the ΔΔCt method and normalized based on β-actin, *P < 0.05, then the logarithmic function analysis was used to assess the correlation. ej RBM38 could bind to c-Myc transcript in vivo in breast cencer cells. eg MCF-7 and hj ZR-75-1 cell lysates were immunoprecipitated with RBM38 antibody or control IgG followed by RT-PCR (e, h) and qRT-PCR (f, g, i, j) measuring the levels of c-Myc, p21 transcripts in the RBM38 or IgG immunocomplexes. Upon normalization with the level of β-actin transcript, these data were calculated from three separate experiments and performed as mean ± SEM, *P < 0.05

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