Fig. 7: Lnc408/CBY1 axis promotes tumorigenesis of BCSCs in vivo. | Cell Death & Disease

Fig. 7: Lnc408/CBY1 axis promotes tumorigenesis of BCSCs in vivo.

From: A novel Lnc408 maintains breast cancer stem cell stemness by recruiting SP3 to suppress CBY1 transcription and increasing nuclear β-catenin levels

Fig. 7

A The tumor initiation and tumor sizes of each group (*P < 0.05, **P < 0.01). B Representative pictures of IHC staining of c-Myc proteins (upper panel) and c-Myc mRNA levels (down panel) in each group (*P < 0.05; scale bar, 50 μm). C Protein levels of nuclear, phosphorylated, and total β-catenin in tumors were determined by western blotting. D Clinical samples were divided into lnc408 high and low expression groups according to lnc408 expression levels, and subjected to western blotting to assess nuclear β-catenin, total β-catenin, and c-Myc expressions. E A schematic model to illustrate lnc408 molecular functions in BCSCs. Lnc408 recruits SP3 to impair CBY1 transcription, the reduced CBY1 lose or significantly incapacitated its ability to form complex with 14-3-3 and β-catenin in CSCs, which notably mitigate the transportation of β-catenin into cytoplasm, to lead an accumulation of nucleus β-catenin, thus triggers the WNT/β-catenin signaling to maintain BCSCs stemness.

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