https://orcid.org/0000-0002-7426-6405
![Sample our Medicine, Dentistry, Nursing & Allied Health journals, sign in here to start your FREE access for 14 days]({"type":"image" , "src" : "/sda/5944/TOC-Subject-Sample-2021-Medicine-Dentistry-Nursing-Allied-Health.jpg"})
Abstract
Background and Aims
Hepatocellular carcinoma (HCC) is a common malignant disease with high morbidity and mortality throughout the world. While Borealin is a putative oncogene that is dysregulated in multiple tumors, its exact role in HCC remains less investigated.
Methods
Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) assays were employed to examine the relative amount of Borealin. Gene set enrichment analysis (GSEA) and other bioinformatic analyses were implemented to probe into the potential functions of Borealin. The biological roles and mechanisms of Borealin in the tumorigenesis and development of HCC were further evaluated using a battery of functional assays in vivo and in vitro.
Results
Borealin was enhanced in the HCC tissue samples and hepatoma cells when compared with the nontumor tissues and normal liver cells. Higher Borealin expression was positively linked with advanced pathological phenotypes and inferior overall survival. The overexpression of Borealin promoted the cells’ abilities on proliferation, invasion and epithelial–mesenchymal transition (EMT) in vitro, facilitated tumor growth and lung metastasis in vivo, whereas the silencing of Borealin inhibited these capabilities in vitro. Furthermore, Borealin interacted with β-catenin and further activated the Wnt/β-catenin signaling pathway, which endowed HCC cells with highly aggressive and metastatic capabilities.
Conclusion
Borealin was identified as an oncogene that could promote HCC growth and metastasis by activating the WNT/β-catenin signaling pathway. These findings extended the understanding of Borealin in HCC tumorigenesis and development and highlighted the significance of Borealin in HCC diagnosis and treatment.
Abbreviations
HCC, hepatocellular carcinoma; mRNA, messenger RNA; WB, Western blotting; IHC, immunohistochemistry; IF, immunofluorescence; CDCA8, cell division cycle associated 8; CPC, chromosomal passenger complex; qRT-PCR, quantitative reverse transcription polymerase chain reaction; cDNA, complementary DNA; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; CCK8, cell counting kit 8; SiRNA, small interference RNA; LIHC, liver hepatocellular carcinoma; GEO, Gene Expression Omnibus; PVTT, portal vein tumor thrombus; BCLC, Barcelona Clinic Liver Cancer; EMT, Epithelial–mesenchymal transition; PVDF, polyvinylidene fluoride; GSEA, gene set enrichment analysis; DEGs, differential expressed genes; SD, standard deviation.
Data Sharing Statement
The data used to support the findings of this study are included within the article and Supplementary files.
Ethical Approval
This study was approved by the Ethical Committee of Xiangyang Central Hospital.
Informed Consent
The human study was known and supported by the Human Subjects Protection Committee of Xiangyang Central Hospital. Animal experiments were approved and supervised by the Animal Ethics Committee of Xiangyang Central Hospital. Written informed consent was obtained from all patients. The study was conducted in accordance with the Declaration of Helsinki.
Acknowledgments
We thank Quanyan Liu, Deliang Guo and Pengpeng Liu for their technical support.
Author Contributions
All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agreed to be accountable for all aspects of the work.
Disclosure
All authors declare no conflicts of interest for this work.