Department of Burns and Plastic Surgery, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
Int J Mol Med. 2019 Mar;43(3):1441-1451. doi: 10.3892/ijmm.2019.4070. Epub 2019 Jan 21.
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.
微小 RNA（miRNAs）通过靶向靶基因的 3'非翻译区（UTR）对基因表达进行转录后调控，在细胞增殖、分化和凋亡中发挥多种作用。然而，miR-16-2-3p 与非综合征性唇裂（NSCL）中 3-磷酸肌醇依赖性蛋白激酶-1（PDPK1）之间的关联尚不清楚。在本研究中，荧光素酶活性测定表明 miR-16-2-3p 在上颌突间充质细胞（MPMCs）中负调控 PDPK1。此外，还证实与相邻正常唇组织相比，裂唇组织中 miR-16-2-3p 的表达水平显著增加。在裂唇组织中观察到 miR-16-2-3p 与 PDPK1 之间存在负相关。此外，miR-16-2-3p 通过抑制 PDPK1 抑制 MPMCs 的增殖和迁移，并诱导其凋亡。最后，miR-16-2-3p 通过抑制 PDPK1/蛋白激酶 B 信号通路在 MPMCs 中发挥其抑制作用。这些结果表明，miR-16-2-3p 可能通过抑制 PDPK1 抑制 MPMCs 的增殖和迁移，并促进其凋亡，可能成为 NSCL 未来临床预防和治疗的潜在靶点。
