ArticleThoracic cancer2018
Oncogenic HBXIP enhances ZEB1 through Sp1 to accelerate breast cancer growth.
Article in Thoracic cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- LAMTOR5 promotes hepatoma growth in mice by disrupting LC3-p62-mediated autophagy and preventing p62 proteasome degradation.Acta pharmacologica Sinica · 2026Article
- ZEB1 and ALKBH5 coregulate CRABP2 and FABP5 and jointly determine the sensitivity of anaplastic thyroid cancers to gemcitabine and retinoic acid.NPJ precision oncology · 2025Article
- Research progress on oncoprotein hepatitis B X‑interacting protein (Review).Molecular medicine reports · 2024Review
- Identification of potential microRNA diagnostic panels and uncovering regulatory mechanisms in breast cancer pathogenesis.Scientific reports · 2022Article
- The modulation of PD-L1 induced by the oncogenic HBXIP for breast cancer growth.Acta pharmacologica Sinica · 2022Article
- ZEB1 directly inhibits GPX4 transcription contributing to ROS accumulation in breast cancer cells.Breast cancer research and treatment · 2021Article
- Construction of a Potential Breast Cancer-Related miRNA-mRNA Regulatory Network.BioMed research international · 2020Article
- The oncoprotein HBXIP facilitates metastasis of hepatocellular carcinoma cells by activation of MMP15 expression.Cancer management and research · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThere is abundant evidence to indicate that HBXIP functions as an oncoprotein and transcription co-activator during the development and promotion of cancers. In multiple cancers, ZEB1 serves as a transcription activator to regulate gene expression. We explored the roles of ZEB1 in HBXIP-induced breast cancer growth.
methodsHBXIP regulation of ZEB1 was evaluated by reverse transcription PCR and immunoblotting. The stimulation of ZEB1 promoter by HBXIP and/or Sp1 was tested using luciferase reporter gene analysis. The alteration of cell proliferation mediated by HBXIP-induced ZEB1 was tested using methyl-thiazolyl-tetrazolium and 5-Ethynyl-2'-deoxyuridine (EdU) incorporation analysis. ZEB1 and HBXIP expression in human breast cancer tissues was analyzed using quantitative real-time PCR. The relationship between HBXIP and ZEB1 was confirmed by Pearson's correlation coefficient.
resultsWe observed dose-dependent upregulation of ZEB1 by HBXIP in breast cancer cells. HBXIP can activate the ZEB1 promoter by interacting with transcription factor Sp1. Cell viability and EdU incorporation analysis showed that HBXIP could drive cell proliferation by enhancing ZEB1 in breast cancer. Using quantitative real-time PCR, ZEB1 overexpression and a positive relationship between ZEB1 and HBXIP were observed in clinical breast cancer samples.
conclusionOncogenic HBXIP controls the transcription regulation of ZEB1 by co-activating Sp1, thereby accelerating breast cancer growth.
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