ArticleJournal of cellular physiology2019
Mutual inhibitions between epidermal growth factor receptor signaling and miR-124a control pancreatic progenitor proliferation.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Potential predictive value of circulating tumor DNA (ctDNA) mutations for the efficacy of immune checkpoint inhibitors in advanced triple-negative breast cancer.Frontiers in genetics · 2023Article
- Metabolic-epigenetic nexus in regulation of stem cell fate.World journal of stem cells · 2022Review
- EGF suppresses the expression of miR-124a in pancreatic β cell lines via ETS2 activation through the MEK and PI3K signaling pathways.International journal of biological sciences · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic stem/progenitor cells convert from a proliferative to a differentiated fate passing through proliferation cease to a resting state. However, the molecular mechanisms of cell cycle arrest are poorly understood. In this study, we demonstrated that the microRNA-124a (miR-124a) inhibited the proliferation of pancreatic progenitor cells both in vitro and ex vivo and promoted a quiescent state. The miR-124a directly targeted SOS Ras/Rac guanine nucleotide exchange factor 1 (SOS1), IQ motif-containing GTPase-activating protein 1 (IQGAP1), signal transducer and activator of transcription 3 (STAT3), and cyclin D2 (CCND2), thereby inactivating epidermal growth factor receptor (EGFR) downstream signaling pathways including mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK), phosphatidylinositol 3-kinase-protein kinase B (PI3K/AKT) and Janus kinase (JAK)/STAT3. miR-124a blocked cell proliferation mainly through targeting STAT3 to inhibit PI3K/AKT and JAK/STAT3 signaling. Moreover, miR-124a expression was negatively regulated by EGFR downstream PI3K/AKT signaling. These results indicated that miR-124a and EGFR signaling mutually interact to form a regulating circuit that determines the proliferation of pancreatic progenitor cells.
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Registered trials
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