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We attempted to investigate the role of HOXB7 in tumor progression and evolution by means of an extensive computer screening analysis of various cancer types. We performed univariate Cox regression and Kaplan-Meier survival analyses to assess the impact of HOXB7 on overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI) in different types of cancer. Furthermore, we examined the relationship between HOXB7 and several clinical features: tumor microenvironment, immune regulatory genes, immune checkpoints, tumor mutational burden (TMB), and microsatellite instability (MSI). We performed gene set enrichment analysis to gain deeper insights into the potential molecular mechanisms of HOXB7, and validated our findings through functional assays in cells, including methyl thiazolyl tetrazolium cytotoxicity and Transwell invasion assays. HOXB7 expression was associated with different clinical characteristics in numerous malignancies. Higher HOXB7 expression was associated with worse OS, DSS, and PFI in some cancer types. In particular, HOXB7 expression was favorably associated with immune cell infiltration, immune regulatory genes, immunological checkpoints, TMB, and MSI in malignancies. Furthermore, we identified a strong link between copper death-associated gene expression and HOXB7 expression. According to the findings of this study, HOXB7 might serve as an appealing focus for tumor diagnosis and immunotherapy and a prospective indicator of prognosis.
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http://dx.doi.org/10.1016/j.compbiomed.2024.108562 | DOI Listing |
JCI Insight
August 2025
Department of Nephrology and Hypertension, Hannover Medical School (MHH), Hannover, Germany.
Mutations in the transcription factor TFAP2A are linked to congenital anomalies of the kidney and urinary tract in humans. While Tfap2a knockout (KO) in mouse collecting ducts leads to tubular epithelial abnormalities, its precise molecular functions in kidney tubules remain unclear. To investigate Tfap2a-dependent gene regulatory networks in the mouse kidney collecting ducts, we employed conditional knockout (Hoxb7-Cre; Tfap2aflox/flox) models combined with transcriptomics.
View Article and Find Full Text PDFNat Commun
August 2025
Department of Pathology, Institute of Systems Biomedicine, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Pancreatic ductal adenocarcinoma (PDAC) poses a serious clinical challenge, demanding further exploration of its pathogenesis and therapeutic targets for metastasis, the main cause of mortality. Here, we identify STN1, a CST complex member crucial for maintaining telomere lengths and genome stability, as a key factor in promoting PDAC metastasis. Elevated STN1 levels correlate with poor patient survival, with oncogenic protein HOXB7 as an upstream transcription factor regulating STN1.
View Article and Find Full Text PDFExpert Rev Anticancer Ther
August 2025
Department of Colorectal Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, People's Republic of China.
Background: Glycosylphosphatidylinositol-anchored proteins (GPI-APs) contribute to cancer progression, with their glycolipid modification mediated by glycosylphosphatidylinositol transamidase (GPIT). Phosphatidylinositol glycan anchor biosynthesis class T (PIGT), a key GPIT subunit, influences GPI-APs biosynthesis and tumor biology. This study investigates PIGT expression in hepatocellular carcinoma (HCC) and its regulatory mechanisms.
View Article and Find Full Text PDFBiochem Biophys Res Commun
September 2025
Department of Biological Science and Technology, Jinzhong University, Jinzhong, 030619, China.
Gastric cancer (GC) is a common solid malignant tumor with a low 5-year survival rate. The underlying mechanism of cisplatin (DDP) resistance in GC cells remains obscure, and therapeutic targets have yet to be identified. Previously, we reported that saikosaponin D (SSD) could increase the DDP sensitivity of the GC cell line SGC-7901.
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