ArticleJournal of the Egyptian National Cancer Institute2025
The decay-accelerating factor (CD55) in acute leukemia patients and its query implication in cancer pathogenesis.
Article in Journal of the Egyptian National Cancer Institute, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Global bibliometric analysis of TP53-mutated acute myeloid leukemia: research hotspots and evolution.Translational cancer research · 2026Article
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Abstract
backgroundThe role of the complement system and its membrane-bound regulatory proteins (mCRPs) in the pathogenesis of cancer is still a debatable issue. The current study aimed to evaluate the role of the complement regulatory protein, the decay-accelerating factor (CD55), in the pathogenesis of acute leukemia.
methodsCD55 gene expression was assessed in the peripheral blood of 34 patients with acute myeloid leukemia (AML), 26 patients with acute lymphoblastic leukemia (ALL), and 30 healthy controls by qRT-PCR. Also, CD55 gene knockdown was performed in HSB-2 (ALL cell line) using customized short hairpin RNA (shRNA). Flowcytometric analysis was done to ensure successful transfection, and MTT assay was performed to evaluate the cell viability post-transfection and silencing of CD55.
resultsThere was a significant downregulation of CD55 in acute leukemia patients compared to the healthy controls (p < 0.001) with RQ values of AML, and ALL patients were 0.2499 ± 0.07427 and 0.2581 ± 0.09467, respectively. The MTT assay showed a significantly reduced viability of HSB-2 cells following posttranscriptional silencing of CD55 (p < 0.001) by 78.6% as compared to the non-transfected or mock-transfected cells. In the presence of human serum, there was a significant reduction in cell viability by 66.3% as compared to non-transfected controls (p = 0.01). Regarding the cells co-transfected with CD55 and CD46 silencing plasmids, cell viability was significantly decreased by 70.6% compared to non-transfected cells.
conclusionCD55 was significantly downregulated in acute leukemia. However, its in vitro silencing showed significant reduction in cell viability, giving it a dual opposing role in cancer.
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