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Validating HMMR Expression and Its Prognostic Significance in Lung Adenocarcinoma Based on Data Mining and Bioinformatics Methods.

ABSTRACT: Hyaluronic acid-mediated motility receptor (HMMR), a tumor-related gene, plays a vital role in the occurrence and progression of various cancers. This research is aimed to reveal the effect of HMMR in lung adenocarcinoma (LUAD). We first obtained the gene expression profiles and clinical data of patients with LUAD from The Cancer Genome Atlas (TCGA) database. Then, based on the TCGA cohort, the HMMR expression difference between LUAD tissues and nontumor tissues was detected and verified with public tissue microarrays (TMAs), clinical LUAD specimen cohort, and Gene Expression Omnibus (GEO) cohort. Logistic regression analysis and chi-square test were adopted to study the correlation between HMMR expression and clinicopathological parameters. The effect of HMMR expression on survival was evaluated by Kaplan-Meier survival analysis and using the Cox regression model. Furthermore, Gene Set Enrichment Analysis (GSEA) was utilized to screen out signaling pathways related to LUAD and the co-expression analysis was employed to build the protein-protein interaction (PPI) network. The HMMR expression level in LUAD tissues was dramatically higher than that in nontumor tissues. Logistic regression analysis and chi-square test demonstrated that the high HMMR expression in LUAD has relation with gender, pathological stage, T classification, lymph node metastasis, and distant metastasis. The Kaplan-Meier curve suggested a poor prognosis for LUAD patients with high HMMR expression. Multivariate analysis implied that the high HMMR expression was a vital independent predictor of poor overall survival (OS). GSEA indicated that a total of 15 signaling pathways were enriched in samples with the high HMMR expression phenotype. The PPI network gave 10 genes co-expressed with HMMR. HMMR may be an oncogene in LUAD and is expected to become a potential prognostic indicator and therapeutic target for LUAD.

SUBMITTER: Li X

PROVIDER: S-EPMC8435795 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background 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). Methods 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. Results 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. Conclusions 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.

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Validating HMMR Expression and Its Prognostic Significance in Lung Adenocarcinoma Based on Data Mining and Bioinformatics Methods.

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