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Research Paper|Volume 11, Issue 17|pp 7123—7149

Chromobox homolog 8 (CBX8) Interacts with Y-Box binding protein 1 (YBX1) to promote cellular proliferation in hepatocellular carcinoma cells

Lushan Xiao1,2,3, Zixiao Zhou1,2,3, Wenwen Li1,2,3, Jie Peng5, Qingcan Sun1,2,3, Hongbo Zhu3,6, Yang Song1,2,3, Jin-Lin Hou1,2,3, Jingyuan Sun1,4, Hui-Chuan Cao1,4, Dong Zhongyi1,4, Dehua Wu1,4, Li Liu1,2,3
  • 1State Key Laboratory of Organ Failure Research, Nan Fang Hospital, Southern Medical University, Guangzhou 510515, China
  • 2Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Nan Fang Hospital, Southern Medical University, Guangzhou 510515, China
  • 3Department of Infectious Diseases, Nan fang Hospital, Southern Medical University, Guangzhou 510515, China
  • 4Department of Radiation Oncology, Nan fang Hospital, Southern Medical University, Guangzhou 510515, China
  • 5Department of Oncology, The Second Affiliated Hospital, Guizhou Medical University, Kaili, P.R. China
  • 6Department of Medical Oncology, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China
* Co-first authors
# Co-senior authors
Received: May 18, 2019Accepted: August 22, 2019Published: September 8, 2019

Copyright © 2019 Xiao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Polycomb group (PcG) proteins have recently been identified as critical regulators in tumor initiation and development. However, the function of CBX8 in human hepatocellular carcinoma (HCC) remains largely unknown. Our study was designed to explore the biological function and clinical implication of CBX8 in HCC. We investigated the interplay between CBX8 and cell cycle through Gene Set Enrichment Analysis and western blotting. Bioinformatics tools and co-immunoprecipitation were used to explore cell cycle regulation. Finally, we studied the expression and clinical significance of CBX8 in HCC through 3 independent datasets. CBX8 was upregulated in HCC and its expression correlated with cell cycle progression. CyclinD1 was downregulated by CBX8 knockdown but upregulated by CBX8 overexpression. YBX1 interacted with CBX8 and regulated the cell cycle. Moreover, targeting YBX1 with specific siRNA impaired CBX8-mediated regulation of CyclinD1. CBX8 overexpression boosted HCC cell growth, while CBX8 knockdown suppressed cell proliferation. Further, YBX1 interacted with CBX8. YBX1 knockdown compromised the proliferation of CBX8 overexpressing cells. CBX8 promotes HCC cell proliferation through YBX1 mediated cell cycle progression and is related to poor HCC prognoses. Therefore, CBX8 may serve as a potential target for the diagnosis and treatment of HCC.