KDM6B overexpression

Finally, KDM6B inhibitor reduced BM repopulating activity of double-lesion mice and tumor burden in mice transplanted with BM-HSPCs from CMML patients with TET2 mutations. These data indicate that TET2 deficiency and KDM6B overexpression cooperate in CMML pathogenesis of and that KDM6B could serve as a potential therapeutic target in this disease.

Notably, the expression of KDM6B in breast cancer tissues was negatively correlated with that of β-catenin, and overexpression of KDM6B decreased the expression of β-catenin and its accumulation in the nucleus of breast cancer cells. Overall, our findings provide novel insights into suppression of metastasis of breast cancer cells by KDM6B via β-catenin, and suggest involvement of the KDM6B-Wnt/β-catenin axis in breast cancer progression.

The present study demonstrated that KDM6B promotes ESCC progression by increasing the transcriptional activity of C/EBPβ depending on its H3K27 demethylase activity.