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HBXIP 通过 PI3K/AKT 和 p53 信号传导调节胃癌葡萄糖代谢和恶性肿瘤
Authors Qiu L, Lu F, Zhang L, Wang G, Geng R, Miao Y
Received 21 December 2019
Accepted for publication 30 March 2020
Published 21 April 2020 Volume 2020:13 Pages 3359—3374
DOI https://doi.org/10.2147/OTT.S243250
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Leo Jen-Liang Su
Introduction: Hepatitis B X-interacting protein (HBXIP) overexpression is related to the progression of multiple cancers. However, its role in gastric cancer (GC) remains unclear.
Materials and Methods: HBXIP expression was determined in human GC specimens and cell lines by quantitative polymerase chain reaction (qRT-PCR) and Western blot. The effects of HBXIP depletion or ectopic expression on GC proliferation were evaluated in vitro using the cell counting kit-8 (CCK-8), 5-ethynyl-2ʹ-deoxyuridine (EdU) incorporation, colony formation, and cell cycle assays. The in vivo effects were investigated using a menograft
model. Apoptosis was evaluated by flow cytometry (in vitro) and
immunohistochemistry (IHC; in vivo). Cell migration and invasion were
evaluated in vitro using wound healing, transwell migration, and
matrigel ouse xinvasion assays; and in vivo by quantifying distant metastases from injection of GC cells in the lateral tail vein.
Results: Herein, we reported that HBXIP expression was higher in GC than in normal tissues, and this high expression indicated a poorer prognosis. Gain- and loss-of-function assays showed that HBXIP promoted GC proliferation, migration, and invasion, and inhibited apoptosis. High-performance liquid chromatography (HPLC) quantification of glycolytic metabolites revealed that HBXIP promoted glucose metabolic reprogramming. Investigation of the PI3K/AKT and p53 pathways highlighted their role in this HBXIP-mediated metabolic reprogramming.
Conclusion: Our results indicate that the up-regulation of HBXIP leads to GC progression by positively regulating glucose metabolism. Therefore, HBXIP is a potential target for the treatment of GC.
Keywords: HBXIP, glucose metabolism, PI3K/AKT, p53, gastric cancer