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Research Paper|Volume 12, Issue 3|pp 3025—3041

Obg-like ATPase 1 (OLA1) overexpression predicts poor prognosis and promotes tumor progression by regulating P21/CDK2 in hepatocellular carcinoma

Shanzhou Huang2, Chuanzhao Zhang2, Chengjun Sun1, Yuchen Hou1, Yixi Zhang1, Nga Lei Tam3, Zekang Wang1, Jia Yu1, Bowen Huang2, Hongkai Zhuang2, Zixuan Zhou2, Zuyi Ma2, Zhonghai Sun2, Xiaoshun He1, Qi Zhou4,5, Baohua Hou2, Linwei Wu1
  • 1Organ Transplant Center, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China
  • 2Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangzhou 510080, China
  • 3The Fifth Affiliated Hospital of Sun Yat-Sen University, Division of Hepatobiliary Surgery, Zhuhai 519000, China
  • 4Department of Liver Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, China
  • 5China Department of General Surgery, Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-Sen University, Huizhou, Guangdong 516081, China
* Equal contribution and co-first authors
Received: November 2, 2019Accepted: January 12, 2020Published: February 11, 2020
https://doi.org/10.18632/aging.102797

Copyright: © 2020 Huang 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

Background: Obg-like ATPase 1 (OLA1) has been found to have a dual role in cancers. However, the relationship between OLA1 and hepatocellular carcinoma (HCC) remains unclear.

Results: High expression of OLA1 in HCC was detected in public datasets and clinical samples, and correlated with poor prognosis. Downregulation of OLA1 significantly inhibited the proliferation, migration, invasion and tumorigenicity of HCC cells. Mechanistically, GSEA showed that OLA1 might promote tumor progression by regulating the cell cycle and apoptosis. In addition, OLA1 knockdown resulted in G0/G1 phase arrest and high levels of apoptosis. OLA1 could bind with P21 and upregulate CDK2 expression to promote HCC progression.

Conclusions: Overall, these findings uncover a role for OLA1 in regulating the proliferation and apoptosis of HCC cells.

Materials and methods: The Cancer Genome Atlas and Gene Expression Omnibus datasets were analyzed to identify gene expression. Immunohistochemistry staining, western blot and real-time polymerase chain reaction were performed to evaluate OLA1 expression in samples. Cell count Kit-8, wound-healing, transwell and flow cytometry assays were used to analyze HCC cell progression. Subcutaneous xenotransplantation models were used to investigate the role of OLA1 in vivo. Coimmunoprecipitation was used to analyze protein interactions.