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Peer-reviewedCC BY 4.0PLOS One

ILF3 regulates erythroid differentiation: A single-cell transcriptomic analysis and cellular experiment

  • Xiaojing Wu1
  • Meng Lu2
  • Wenguang Jia3
  • Weixiong Lin4
  • Yunyan He
4 affiliations
  1. 1Department of Pediatrics, The First Affiliated Hospital of Guangxi Medical University, Nanning, China
  2. 2Graduate School, Guangxi Medical University, Nanning, China
  3. 3NHC Key Laboratory of Thalassemia Medicine, Chinese Academy of Medical Sciences, Nanning, China
  4. 4Guangxi Key Laboratory of Thalassemia Research, Nanning, China
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Abstract

Background: Despite extensive knowledge of erythropoiesis, the role of interleukin enhancer binding factor 3 (ILF3) in β-thalassemia remains unclear. The aim of this study was to investigate the expression pattern and functional role of ILF3 during erythroid differentiation in β-thalassemia. Methods: (1) Single-cell transcriptomic profiles were constructed based on the GSE133181 dataset (3 healthy controls and 3 β-thalassemia patients). The differential expression of ILF3, transcriptional programs of erythroid subsets, pathway activity, and differentiation trajectory were analyzed. (2) ILF3 was knocked out in K562 cells using sgRNA. Cell proliferation was detected by CCK-8 assay, and apoptosis was measured by Annexin V-APC single staining. Results: (1) ILF3 was downregulated in the β-thalassemia group, and the proportion of erythroid cells was significantly enriched in ILF3+ cells. (2) ILF3+ erythroid cells highly expressed maturation-related genes and were enriched in cell cycle and metabolic synthesis pathways, while ILF3− cells highly expressed stress-related genes and activated inflammatory stress pathways. (3) Trajectory analysis suggested early arrest of erythroid differentiation in β-thalassemia, with consistently low ILF3 expression throughout the disease group. (4) Knockout of ILF3 promoted apoptosis in K562 cells. Conclusion: ILF3 is downregulated in β-thalassemia, and its deficiency may contribute to erythroid differentiation arrest and ineffective hematopoiesis by inducing apoptosis and potentially enhancing inflammatory stress.

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Cite

BibTeXRIS
BibTeX
@article{wu2026ilf3,
  title = {{ILF3 regulates erythroid differentiation: A single-cell transcriptomic analysis and cellular experiment}},
  author = {Xiaojing Wu and Meng Lu and Wenguang Jia and Weixiong Lin and Yunyan He},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0355975},
  url = {https://doi.org/10.1371/journal.pone.0355975},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - ILF3 regulates erythroid differentiation: A single-cell transcriptomic analysis and cellular experiment
AU  - Xiaojing Wu
AU  - Meng Lu
AU  - Wenguang Jia
AU  - Weixiong Lin
AU  - Yunyan He
PY  - 2026
DA  - 2026/09/03
JO  - PLOS One
DO  - 10.1371/journal.pone.0355975
UR  - https://doi.org/10.1371/journal.pone.0355975
AB  - Background: Despite extensive knowledge of erythropoiesis, the role of interleukin enhancer binding factor 3 (ILF3) in β-thalassemia remains unclear. The aim of this study was to investigate the expression pattern and functional role of ILF3 during erythroid differentiation in β-thalassemia. Methods: (1) Single-cell transcriptomic profiles were constructed based on the GSE133181 dataset (3 healthy controls and 3 β-thalassemia patients). The differential expression of ILF3, transcriptional programs of erythroid subsets, pathway activity, and differentiation trajectory were analyzed. (2) ILF3 was knocked out in K562 cells using sgRNA. Cell proliferation was detected by CCK-8 assay, and apoptosis was measured by Annexin V-APC single staining. Results: (1) ILF3 was downregulated in the β-thalassemia group, and the proportion of erythroid cells was significantly enriched in ILF3+ cells. (2) ILF3+ erythroid cells highly expressed maturation-related genes and were enriched in cell cycle and metabolic synthesis pathways, while ILF3− cells highly expressed stress-related genes and activated inflammatory stress pathways. (3) Trajectory analysis suggested early arrest of erythroid differentiation in β-thalassemia, with consistently low ILF3 expression throughout the disease group. (4) Knockout of ILF3 promoted apoptosis in K562 cells. Conclusion: ILF3 is downregulated in β-thalassemia, and its deficiency may contribute to erythroid differentiation arrest and ineffective hematopoiesis by inducing apoptosis and potentially enhancing inflammatory stress.
SN  - 1932-6203
ER  -