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Nuclear factor-κB p65 regulates glutaminase 1 expression in human hepatocellular carcinoma

Authors Dong M, Miao L, Zhang F, Li S, Han J, Yu R, Qie S

Received 6 March 2018

Accepted for publication 8 May 2018

Published 28 June 2018 Volume 2018:11 Pages 3721—3729


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Samir Farghaly

Meng Dong,1 Lin Miao,2 Fengmei Zhang,3 Shengshui Li,3 Jingzhi Han,1 Ruohui Yu,1 Shuo Qie4

1Department of Hepatobiliary Surgery, Hebei Cangzhou Hospital of Integrated Traditional Chinese and Western Medicine, Cangzhou, Hebei 061001, China; 2Departments of Obstetrics and Gynecology, Yixingbu Hospital, Beichen, Tianjin 300402, China; 3Department of Pathology, Hebei Cangzhou Hospital of Integrated Traditional Chinese and Western Medicine, Cangzhou, Hebei 061001, China; 4Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA

Background: Glutaminase (GLS), the key enzyme that catalyzes glutamine catabolism, facilitates the production of energy, building blocks, and factors resisting stresses. Two isoforms of GLS have been identified: GLS1 and GLS2. Elevated GLS1 contributes to tumorigenesis and tumor progression. This study investigates the molecular mechanism by which GLS1 is regulated in human hepatocellular carcinoma (HCC).
Methods: Online databases were investigated to search for factors that co-overexpress with GLS1. siRNA knockdown or chemical compounds were utilized to manipulate the activation or inactivation of nuclear factor-κB (NF-κB) p65 signaling. Both the mRNA and protein levels of GLS1 were detected. The biological and clinical importance of p65-GLS1 in HCC was also demonstrated.
Results: NF-κB p65 regulates GLS1 expression in HCC cells. Knockdown or suppression of GLS1 compromises HCC cell proliferation. Elevated GLS1 expression correlates with neoplasm histological grade, and the dysregulation of p65-GLS1 is associated with poor prognosis in human HCC patients.
Conclusion: GLS1 can be developed as a diagnostic and therapeutic target for human HCC.

hepatocellular carcinoma, NF-κB p65, glutaminase, proliferation, prognosis

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