ArticleJournal of Cancer2023
FOXP1-GINS1 axis promotes DLBCL proliferation and directs doxorubicin resistance.
Article in Journal of Cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- PRMT7-mediated arginine methylation of FOXK activates Wnt/β-catenin signalling to drive doxorubicin resistance in diffuse large B-cell lymphoma.Clinical and translational medicine · 2026Article
- P300 enhances glycolysis and dox resistance in DLBCL by upregulating HK2 expression through histone lactylation.BMC cancer · 2026Article
- Upregulation of itchy E3 ubiquitin protein ligase contributes to endometrial cancer through promoting forkhead box P1 degradation.CytoJournal · 2026Article
- Mechanisms of first-line treatment resistance in diffuse large B-cell lymphoma.Frontiers in immunology · 2026Review
- The Role of Chemokine-Related Genes in Diffuse Large B-Cell Lymphoma Prognosis and Tumor Microenvironment Characteristics.Analytical cellular pathology (Amsterdam) · 2026Article
- PAX Family, Master Regulator in Cancer.Diagnostics (Basel, Switzerland) · 2025Review
- GINS1 facilitates the development of lung adenocarcinoma via Wnt/β-catenin activation.World journal of surgical oncology · 2025Article
- FOXP1 is associated with oncogenesis and clinical outcomes in hematologic malignancies.Frontiers in immunology · 2025Article
- An integrated analysis of the anticarcinogenic role of forkhead box protein 1 in oesophageal squamous cell carcinoma.Journal of cellular and molecular medicine · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GINS1 is overexpressed in several types of cancers including leukemia and linked to poor outcomes. However, GINS1 remains poorly investigated in DLBCL (diffuse large B-cell lymphoma). This project aimed to explore the expression, functions and regulation of GINS1 in DLBCL. In this study, through analysis of clinical specimens from DLBCL patients, we uncovered that GINS1 was upregulated in DLBCL. By EMSA, ChIP and luciferase reporter assays, it was found that FOXP1 transcriptionally activated GINS1 expression by directly binding to the promoter region of the GINS1 gene. Western blotting and RT-PCR also revealed that GINS1 expression positively correlated with FOXP1 in human DLBCL specimens and cell lines. In an in vivo xenograft lymphoma mouse model, the FOXP1/GINS1 regulatory axis was also validated. Moreover, with CCK8 cell proliferation assays and colony formation assay, elevated GINS1 expression was found to be associated with doxorubicin resistance in lymphoma cells. Our findings showed that the FOXP1-GINS1 axis played a critical role in DLBCL development and doxorubicin resistance, and targeting the FOXP1-GINS1 axis could be a potential therapeutic approach for DLBCL treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.