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Marker of proliferation Ki-67 expression is associated with transforming growth factor beta 1 and can predict the prognosis of patients with hepatic B virus-related hepatocellular carcinoma

Authors Yang C, Su H, Liao X, Han C, Yu T, Zhu G, Wang X, Winkler CA, O'Brien SJ, Peng T

Received 15 January 2018

Accepted for publication 9 February 2018

Published 10 April 2018 Volume 2018:10 Pages 679—696

DOI https://doi.org/10.2147/CMAR.S162595

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Leylah Drusbosky


Chengkun Yang,1,* Hao Su,1,* Xiwen Liao,1 Chuangye Han,1 Tingdong Yu,1 Guangzhi Zhu,1 Xiangkun Wang,1 Cheryl Ann Winkler,2 Stephen J O’Brien,3–5 Tao Peng1

1Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Province, China; 2Basic Research Laboratory, CCR, NCI, Leidos Biomedical Research, Frederick National Laboratory, Frederick, MD, USA; 3Laboratory of Genomic Diversity, National Cancer Institute, NIH, Frederick, MD, USA; 4Theodosius Dobzhansky Center for Genome Bioinformatics, St. Petersburg State University, St Petersburg, Russia; 5Guy Harvey Oceanographic Center, Halmos College of Natural Sciences and Oceanography, Nova Southeastern University, Fort Lauderdale, FL, USA

*These authors contributed equally to this work


Abstract:
Hepatocellular carcinoma (HCC) is the most frequent malignancy of the liver. Transforming growth factor beta 1 (TGFB1) and marker of proliferation Ki-67 (MKI67) regulate cell proliferation, differentiation, and growth. The association between MKI67 and TGFB1 expression and its clinical implications in HCC remain unknown.
Methods: Public databases were used to analyze TGFB1 and MKI67 expression in different pathologic grades/stages and tissue types of HCC. The association between MKI67 and TGFB1 expression was explored using pathway analysis and in a HepG2 cell line treated with TGFB1. Survival analysis was performed to evaluate the prognostic value of TGFB1 and MKI67 expression in patients with hepatitis B virus (HBV)-related HCC.
Results: We identified that MKI67 expression was upregulated in liver cancer tissues. MKI67 and TGFB1 expression levels were different in various stages and tissue types of liver cancer. Furthermore, MKI67 expression was associated with TGFB1 expression in liver cancer tissues and HepG2 cells. Patients with HBV-related HCC and a higher level of MKI67 expression had a worse prognosis. Moreover, a nomogram was conducted to predict the clinical outcomes of patients with HBV-related HCC.
Conclusion: MKI67 expression level was associated with TGFB1 expression in liver cancer tissues and a HepG2 cell line. MKI67 expression level can predict the clinical outcomes of patients with HBV-related HCC.

Keywords: MKI67, TGFB1, HBV-related HCC, nomogram

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