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Prognostic significance of HSF2BP in lung adenocarcinoma.

  • Huang, Zhendong1
  • Liu, Zhendong2
  • Cheng, Xingbo2
  • Han, Zhibin2
  • Li, Jiwei1
  • Xia, Tian1
  • Gao, Yanzheng2
  • Wei, Li1
  • 1 Department of Thoracic Surgery, Zhengzhou Key Laboratory for Surgical Treatment for End-Stage Lung Disease, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, China. , (China)
  • 2 Department of Surgery of Spine and Spinal Cord, Henan Provincial People's Hospital, Henan International Joint Laboratory of Intelligentized Orthopedics Innovation and Transformation, Henan Key Laboratory for Intelligent Precision Orthopedics, Zhengzhou University People's Hospital, People's Hospital of Henan University, Zhengzhou, China. , (China)
Published Article
Annals of Translational Medicine
AME Publishing Company
Publication Date
Oct 01, 2021
DOI: 10.21037/atm-21-4935
PMID: 34790765


Recent studies have demonstrated that upregulation of heat shock transcription factor 2 binding protein (HSF2BP) may promote genomic instability, thereby leading to the development of tumors and also providing a potential target for biological antitumor therapy. However, the role of HSF2BP has so far remained unclear in lung adenocarcinoma (LUAD). To explore the function of HSF2BP in LUAD, we collected transcriptome data for 551 lung samples from The Cancer Genome Atlas (TCGA) database and methylation data for 461 lung samples from the University of California Santa Cruz (UCSC) genome database, in addition to corresponding clinical information. We used bioinformatic approaches to systematically explore the role of HSF2BP in LUAD, including Gene Set Enrichment Analysis (GSEA), coexpression analysis, the Tumor IMmune Estimation Resource (TIMER) tool, Connectivity Map (CMap) analysis, and a meta-analysis involving three Gene Expression Omnibus (GEO) datasets and one TCGA dataset. Our results found that upregulation of HSF2BP in LUAD was an independent risk factor for the prognosis and diagnosis of LUAD. GSEA analysis showed HSF2BP expression was associated with vital signaling pathways, including the cell cycle, P53 signaling pathway, and homologous recombination. Coexpression analysis revealed 10 HSF2BP-associated genes, including oncogenes and tumor suppressor genes. Additionally, we found that HSF2BP expression was negatively correlated with B-cell infiltration and had a potential interaction with CD80 in LUAD, which may play an important role in tumor immune escape. Finally, we identified four small-molecule drugs which show promise for LUAD treatment. The present study found that elevated HSF2BP posed a threat to prognosis in LUAD patients. HSF2BP might have been involved in tumorigenesis by influencing genomic stability and contributing to tumor immune evasion in the tumor immune microenvironment of LUAD. These findings suggest that HSF2BP may provide a vulnerable target for improving and enhancing treatment of LUAD. 2021 Annals of Translational Medicine. All rights reserved.

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