ArticleOncoTargets and therapy2020
HBXIP Regulates Gastric Cancer Glucose Metabolism and Malignancy Through PI3K/AKT and p53 Signaling.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- The association of HBV infection and head and neck cancer: a systematic review and meta-analysis.BMC cancer · 2024Pooled it
- An overview of hepatitis B virus in gastric carcinogenesis: from clinical association to molecular mechanisms.Infectious agents and cancer · 2025Review
- Comprehensive analysis of prognosis and drug sensitivity of programmed cell death pattern-related genes in gastric cancer patients.Scientific reports · 2025Article
- [Occurrence risk of extrahepatic liver tumor with hepatitis B virus infection].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025Review
- Sphingolipid Metabolism Dysregulation Drives Immune Microenvironment Remodeling and Predicts Prognosis in Bladder Cancer.International journal of genomics · 2025Article
- Alkaloids of Aconiti Lateralis Radix Praeparata inhibit growth of non-small cell lung cancer by regulating PI3K/Akt-mTOR signaling and glycolysis.Communications biology · 2024Article
- Research progress on oncoprotein hepatitis B X‑interacting protein (Review).Molecular medicine reports · 2024Review
- Energy metabolism: a new target for gastric cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- Evodiamine Inhibits Colorectal Cancer Growth via RTKs Mediated PI3K/AKT/p53 Signaling Pathway.Journal of Cancer · 2024Article
- Exploring the Microbiome in Gastric Cancer: Assessing Potential Implications and Contextualizing Microorganisms beyondCancers · 2023Review
- [High expression of MRPL13 promotes cell cycle progression and proliferation of gastric cancer cells by inhibiting p53 signaling to affect long-term prognosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- HBXIP knockdown inhibits FHL2 to promote cycle arrest and suppress cervical cancer cell proliferation, invasion and migration.Oncology letters · 2023Article
- The Identification and Clinical Value Evaluation of CYCS Related to Asthma through Bioinformatics Analysis and Functional Experiments.Disease markers · 2023Article
- Hepatitis B virus infection: An insight into the clinical connection and molecular interaction between hepatitis B virus and host extrahepatic cancer risk.Frontiers in immunology · 2023Review
- Evaluation of aliphatic acid metabolism in bladder cancer with the goal of guiding therapeutic treatment.Frontiers in oncology · 2022Article
- Isoforms of the p53 Family and Gastric Cancer: A Ménage à Trois for an Unfinished Affair.Cancers · 2021Review
- HBXIP promotes gastric cancerAging · 2020Article
- STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects.Biology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionHepatitis 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
methodsHBXIP 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-2'-deoxyuridine (EdU) incorporation, colony formation, and cell cycle assays. The in vivo effects were investigated using a mouse xenograft 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 invasion assays; and in vivo by quantifying distant metastases from injection of GC cells in the lateral tail vein.
resultsHerein, 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.
conclusionOur 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.
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Registered trials
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