ArticleFrontiers in immunology2025
Ribosomal protein L9 is a potential therapeutic target for B-ALL through the activation of the p53 signaling pathway.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Comprehensive bioinformatics analysis and clinical validation of PPP1R13L in rectal adenocarcinoma.BMC cancer · 2026Article
- Altered Expression of Ribosome Biogenesis Regulators (TP53, C-MYC, FBL, and NCL) in Precursor B-cell Acute Lymphoblastic Leukemia and Neuroblastoma.Current issues in molecular biology · 2026Article
- Association Between Amino Acid Polymorphisms in MICA and MICA-NKG2D Interaction Affinity: Implications and Significance for Tumor Immunity.Biomolecules · 2025Review
- Immunometabolic Dysregulation in B-Cell Acute Lymphoblastic Leukemia Revealed by Single-Cell RNA Sequencing: Perspectives on Subtypes and Potential Therapeutic Targets.International journal of molecular sciences · 2025Article
- Silencing RPL9 promotes malignant proliferation in breast cancer cells.International journal of immunopathology and pharmacologyArticle
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Authors and funding
7 authors.
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Abstract
B-cell acute lymphocytic leukemia (B-ALL) is a malignant hematological disorder marked by the aberrant proliferation of abnormal B lymphocytes. Although recent advancements have highlighted the pivotal role of ribosomes in the progression of B-ALL, the specific function of ribosomal protein L9 (RPL9), a key component of ribosomal structural protein, still unclear. In this study, we observed a significant upregulation of RPL9 in human B-ALL cells compared to normal B cells, suggesting RPL9's potential key role in B-ALL progression. Enforced RPL9 knockdown (KD) led to decreased proliferation and increased apoptosis in B-ALL cells compared to the control group. Furthermore, RPL9 KD significantly extended the survival time of NCG mice bearing B-ALL cells
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