Fig. 3
From: The role of kinesin family members in hepatobiliary carcinomas: from bench to bedside
The roles of the kinesin-5, 6 family members in HCC. (A) Kinesin-5 family: a reciprocal feedback loop exists between KIF11 and PAK6 and impacts tumor proliferation, invasion, and migration, both PAK6-inhibition or KIF11-overexpression can enhance tumor cells motility and viability. Similarly, the abnormal spindle-like microcephaly-associated protein (ASPM) also negatively modulates KIF11 expression, and the regulatory effects of the ASPM/KIF11 signaling on tumor proliferation, invasion, and migration may be linked to WNT/β-catenin signaling transduction. (B) Kinesin-6 family: For KIF20A, identified as an effector in the Hedgehog (Hh) signaling that could be indirectly transcriptional up-regulated by Gli2, acting via FOXM1. For KIF23, exerted as an up- or downstream regulator of three major axes including YAP/TAZ, p53, and WNT/β-catenin signaling pathways with an impact on HCC. Besides, KIF23 could also be recognized and repressed by miR-424-5p, or inhibited by FOXM1 silencing, which was attributed to reduced acetylation level of histone H3 lysine 27 (H3K27ac) at the promoter of KIF23