Kinesin Family Member C1 (KIFC1) Accelerates Proliferation andInvasion of Endometrial Cancer Cells Through Modulating the PI3K/AKT SignalingPathway

摘要

Endometrial cancer (EC) is one of the most common cancers among women worldwide.Kinesin family member C1 (KIFC1) has been demonstrated to play crucial roles invarious tumors. However, the function of KIFC1 in EC remains to be revealed. Inthis study, upregulation of KIFC1 expression in human EC tissues was found fromanalysis on data from The Cancer Genome Atlas (TCGA), and positively correlatedwith short survival outcome of EC patients. In addition, the mRNA and proteinlevels of KIFC1 were confirmed to be up-regulated in EC cells (Ishikawa, HEC-1B,HEC-1A and KLE) compared to human normal endometrial stromal cells (hESCs) byquantitative real time PCR and western blot. In vitrofunctional experiments showed that overexpression of KIFC1 promotedproliferation, migration and invasion of EC cells, while KIFC1 depletion showedthe opposite results. Moreover, KIFC1 knockdown suppressed tumor growth in mice.Further mechanism analysis showed that KIFC1 participated in the regulation ofEC progression through regulating the PI3K/AKT signaling pathway. Collectively,KIFC1 promoted proliferation and invasion through modulating PI3K/AKT signalingpathway in EC, implying that KIFC1 might provide a promising therapeutic targetfor the therapy of EC.