Fig. 6: Decreased expression of CTTNBP2 and MCF2L is correlated with more adverse prognostic characteristics and an enhanced tumorigenic phenotype in cells.
From: Regulatory non-coding somatic mutations as drivers of neuroblastoma
a CTTNBP2 (left) and MCF2L (right) expression by clinical features. From the top, risk group, MYCN amplification and INSS Stage. b In LAN-2 cells transfected with three pooled CTTNBP2 siRNA, CTTNBP2 expression relative to siScramble (scramble), as measured by western blot (left) and qPCR (right) 24 h, 48 h and 72 h post CTTNBP2 silencing. c SK-N-BE(2) cells transfected with three pooled MCF2L siRNA, MCF2L expression relative to siScramble (scramble), as measured by western blot (left) and qPCR (right) 24 h, 48 h and 72 h post MCF2L silencing. β-Actin protein levels are used as loading control. d Cell viability assays in LAN-2 (left) and SK-N-BE(2) (right) cells silenced for CTTNBP2 and MCF2L respectively, are shown as fold change compared to wild-type cells. e Invading cells number of LAN-2 (left) and SK-N-BE(2) (right) silenced for CTTNBP2 and MCF2L respectively, are shown as fold change compared to wild-type cells. Representative images (10×) of invasion assays in silenced cells are reported on the right. All data shown are the mean ± standard deviation from three independent qPCR experiments, each done in triplicate. Significant p-values obtained by two-tailed T-test are reported by * (* < 0.05; ** < 0.01; *** < 0.001).
