Here, we demonstrate that two cullin genes, CUL4A and CUL4B, but not other members, are specifically overexpressed in CAC tumour samples and positively correlate with levels of the proinflammatory cytokines IL-1β and IL-6.
Previous studies have revealed that CUL4B is overexpressed in various types of cancer and that its overexpression is related to the progression and metastasis of tumors.
Taken together, these data reveal CRL4B<sup>RBBP7</sup> is the E3 ligase responsible for the proteasomal degradation of HUWE1, and further provide a potential strategy for cancer therapy by targeting HUWE1 and the CUL4B E3 ligase complex.
We conclude that CUL4B can up-regulate Wnt/β-catenin signalling in human HCC through transcriptionally repressing Wnt antagonists and thus contributes to the malignancy of HCC.