Abstract
Chemerin is a newly described adipokine with significant effects on obesity, metabolic disorders, and immune trafficking. Recently, chemerin has gained prominence for its potential roles in cancer and tumorigenesis with pro‐ or antitumor effects. To date, most referenced multifunctions of chemerin are attributed to the chemokine‐like receptor 1 (CMKLR1), distributing broadly in many tissues. This study investigates the in vitro roles of chemerin treatment on migration and invasion of ovarian carcinoma cells (OVCAR‐3 and SK‐OV‐3) and potential underlying mechanisms. Herein, exogenous chemerin treatment promotes growth and invasion of SK‐OV‐3 cells but has no significant effects on OVCAR‐3 cells. SK‐OV‐3 cells undergo morphological elongation characterized by epithelial‐to‐mesenchymal transition (EMT) and Ras homologous genome members A (RhoA)/Rho protein‐related curl spiral kinase‐1 (ROCK1) activation. Furthermore, chemerin‐enhanced invasion and EMT of SK‐OV‐3 cells are effectively blocked by C3 transferase (C3T) and Y27632 and RhoA and ROCK1 inhibitor, respectively. More importantly, RhoA/ROCK1‐EMT‐mediated SK‐OV‐3 cell invasion is orchestrated by CMKLR1 upregulation after chemerin treatment (50 ng/mL). The silencing of CMKLR1 significantly (P < 0.0001) reverses the chemerin‐enhanced invasion, EMT, and RhoA/ROCK1 activation of SK‐OV‐3 cells. Our study indicates that chemerin promotes invasion of OC cells via CMKLR1‐RhoA/ROCK1‐mediated EMT, offering a novel potential target for metastasis of OC.