Skip to main content
Fig. 8 | Molecular Cancer

Fig. 8

From: MASTL induces Colon Cancer progression and Chemoresistance by promoting Wnt/β-catenin signaling

Fig. 8

MASTL imparts chemoresistance to 5-FU in colon cancer cell lines. (a) HCT116C and HCT116MKD cells were treated with 10 and 20 μM of 5-FU. Western blot analysis demonstrated induction of Survivin and Bcl-xL in control cells. However, inhibition of MASTL inhibited these protein expression even in presence of 5-FU. (b) MTT assay in HCT116C and HCT116MKD cells showed significant reduction in viable cells as compared to control treated cells. For graphs, data represent mean ± SD; **, P < 0.001; ***, P < 0.0001 versus control. (c) Model depicting the role of MASTL in regulation of colon cancer progression. When MASTL expression is increased it phosphorylates GSK-3β and inactivates it, thereby β-catenin is not phosphorylated and degraded. The β-catenin then is translocated into nucleus leading to active transcription of its target genes c-Myc, Survivin and Bcl-xL. These cells escape G2M arrest and apoptosis leading to cancer progression. Conversely, in MASTL inhibited cells, GSK-3β is active which then phosphorylates and degrades β-catenin thus preventing its translocation to nucleus and activation of target genes

Back to article page