NPFFR2 Contributes to the Malignancy of Hepatocellular Carcinoma Development by Activating RhoA/YAP Signaling

Author:

Shin YunaORCID,Jung Wonhee,Kim Mi-Yeon,Shin Dongjo,Kim Geun Hee,Kim Chun Ho,Park Sun-Hoo,Cho Eung-Ho,Choi Dong Wook,Han Chul Ju,Lee Kee Ho,Kim Sang-Bum,Shin Hyun Jin

Abstract

G protein–coupled receptors (GPCRs) are a diverse family of cell surface receptors implicated in various physiological functions, making them common targets for approved drugs. Many GPCRs are abnormally activated in cancers and have emerged as therapeutic targets for cancer. Neuropeptide FF receptor 2 (NPFFR2) is a GPCR that helps regulate pain and modulates the opioid system; however, its function remains unknown in cancers. Here, we found that NPFFR2 is significantly up-regulated in liver cancer and its expression is related to poor prognosis. Silencing of NPFFR2 reduced the malignancy of liver cancer cells by decreasing cell survival, invasion, and migration, while its overexpression increased invasion, migration, and anchorage-independent cell growth. Moreover, we found that the malignant function of NPFFR2 depends on RhoA and YAP signaling. Inhibition of Rho kinase activity completely restored the phenotypes induced by NPFFR2, and RhoA/F-Actin/YAP signaling was controlled by NPFFR2. These findings demonstrate that NPFFR2 may be a potential target for the treatment of hepatocellular carcinoma.

Funder

Korea Institute of Radiological and Medical Sciences

National Research Foundation of Korea

Publisher

MDPI AG

Subject

Cancer Research,Oncology

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