ArticleOncology reports2020
IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Advances in the role of the IGF signaling system in myelodysplastic syndromes and acute myeloid leukemia.Frontiers in oncology · 2025Review
- Mesenchymal Stem Cells in Myelodysplastic Syndromes and Leukaemia.Biomedicines · 2024Review
- CircOMA1 promotes tumour growth and metastasis of bladder cancer by modulating IGF-IR/MAPK/EMT pathway.Clinical and translational medicine · 2022Article
- LncRNA BC200/miR-150-5p/MYB positive feedback loop promotes the malignant proliferation of myelodysplastic syndrome.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 insulin‑like growth factor receptor (IGF‑IR) signaling is considered to serve a key role in the development of cancer. However, the effects of IGF‑IR on the malignant characteristics of myelodysplastic syndrome (MDS) clonal cells remains to be determined. In the present study it was demonstrated that knockdown of IGF‑IR reduced the proliferation and increased the apoptosis of MDS/leukemia cells. Integrated analysis of gene expression profiles using bioinformatics identified the MAPK signaling pathway as a critical downstream factor of IGF‑IR, and this was confirmed in vitro using western blotting which revealed that IGF‑IR knockdown significantly increased the expression of activated MAPK. Furthermore, IGF‑IR signaling was inhibited to investigate the potential of IGF‑IR as a therapeutic target of MDS. The results revealed that the IGF‑IR inhibitor picropodophyllin (PPP) inhibited cell proliferation, promoted cell apoptosis and arrested the cell cycle at the G2/M phase in MDS/leukemia cells. Similar to the effects of IGF‑IR knockdown, PPP treatment also increased MAPK signaling in vitro. In conclusion, IGF‑IR may serve as a potential therapeutic target of MDS.
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Registered trials
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