ArticleLeukemia2020
Altered expression of CSF3R splice variants impacts signal response and is associated with SRSF2 mutations.
Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Targeting RNA splicing modulation: new perspectives for anticancer strategy?Journal of experimental & clinical cancer research : CR · 2025Review
- Article
- Function of serine/arginine-rich splicing factors in hematopoiesis and hematopoietic malignancies.Cancer cell international · 2024Review
- Upregulation of MMPs in placentas of patients with gestational diabetes mellitus: Involvement of the PI3K/Akt pathway.Heliyon · 2024Article
- SRSF2 is required for mRNA splicing during spermatogenesis.BMC biology · 2023Article
- Towards understandings of serine/arginine-rich splicing factors.Acta pharmaceutica Sinica. B · 2023Review
- Article
- An ensemble machine learning model based on multiple filtering and supervised attribute clustering algorithm for classifying cancer samples.PeerJ. Computer science · 2021Article
- Splicing factor SRSF2-centric gene regulation.International journal of biological sciences · 2021Review
- Cytokine receptor splice variants in hematologic diseases.Cytokine · 2020Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Three annotated CSF3R mRNA splice variants have been described. CSF3R-V1 is the wild-type receptor, while CSF3R-V4 is a truncated form increased in some patients with AML. CSF3R-V3 mRNA was identified in placenta more than 20 years ago, but remains largely uncharacterized due to the lack of a suitable detection assay. Using a novel digital PCR method to quantitate expression of each CSF3R mRNA splice variant in hematopoietic cells, CSF3R-V1 was most highly expressed followed by CSF3R-V3. Functional assays revealed expression of V3 alone conferred a hypoproliferative phenotype associated with defective JAK-STAT activation. However, coexpression of V1 with V3 rescued proliferative responses. Comparative analysis of V3/V1 expression in CD34+ cells from healthy donors and patients with AML revealed a statistically significant increase in the V3/V1 ratio only in the subset of patients with AML harboring SRSF2 mutations. Knockout of SRFS2 in KG-1 and normal CD34+ cells decreased the V3/V1 ratio. Collectively, these data are the first to demonstrate expression of the CSF3R-V3 splice variant in primary human myeloid cells and a role for SRSF2 in modulating CSF3R splicing. Our findings provide confirmatory evidence that CSF3R is a target of SRSF2 mutations, which has implications for novel treatment strategies for SRSF2-mutated myeloid malignancies.
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