ArticleInternational journal of molecular medicine2019
miR‑16‑2‑3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Computational identification of putative mRNA-miRNA signatures in chemoresistant and metastatic triple-negative breast cancer.Biochemistry and biophysics reports · 2026Article
- Review
- MicroRNAs in maxillofacial bone modeling and remodeling: implications for malocclusion development and orthodontic treatment.Frontiers in cell and developmental biology · 2024Review
- Expansion of plasma MicroRNAs over the first month following human stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Sedentary and Trained Older Men Have Distinct Circulating Exosomal microRNA Profiles at Baseline and in Response to Acute Exercise.Frontiers in physiology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) post‑transcriptionally regulate gene expression by targeting the 3' untranslated region (UTR) of target genes, and serve diverse roles in cell proliferation, differentiation and apoptosis. However, the association between miR‑16‑2‑3p and 3‑phosphoinositide‑dependent protein kinase‑1 (PDPK1) in nonsyndromic cleft lip (NSCL) remains unclear. In the present study, a luciferase activity assay indicated that miR‑16‑2‑3p negatively regulated PDPK1 in maxillary primordium mesenchymal cells (MPMCs). In addition, it was confirmed that the expression levels of miR‑16‑2‑3p was markedly increased in cleft lip tissues compared with those in adjacent normal lip tissues. A negative correlation between miR‑16‑2‑3p and PDPK1 in cleft lip tissues was observed. Furthermore, miR‑16‑2‑3p inhibited cell proliferation and migration, and induced apoptosis of MPMCs via repressing PDPK1. Finally, miR‑16‑2‑3p exerted its suppressive role in MPMCs by inhibiting the PDPK1/protein kinase B signaling pathway. These results indicate that miR‑16‑2‑3p may inhibit cell proliferation and migration, and promote apoptosis in MPMCs through repression of PDPK1 and may be a potential target for future clinical prevention and treatment of NSCL.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.