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 . 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 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.
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| http://dx.doi.org/10.2147/OTT.S167408 | DOI Listing |
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