miR‑15a‑3p affects the proliferation, migration and apoptosis of lens epithelial cells

Mol Med Rep. 2019 Feb;19(2):1110-1116. doi: 10.3892/mmr.2018.9738. Epub 2018 Dec 11.

Abstract

The present study investigated the effect of microRNA (miR)‑15a‑3p on the proliferation, migration and apoptosis of lens epithelial cells and its potential mechanism, in order to further elucidate the pathogenesis of age‑related cataracts (ARCs). The HLE‑B3 human lens epithelial cell line was transfected with miR‑15a‑3p mimic. Expression of the miR‑15a‑3p mimic was measured by fluorescence‑based reverse transcription‑quantitative polymerase chain reaction analysis. Cell proliferation, apoptosis, invasion and migration were investigated using MTT and plate clone formation assays, terminal deoxynucleotidyl transferase dUTP nick end labeling and flow cytometry, and a wound healing assay and Transwell assay, respectively. The protein expression levels of B‑cell lymphoma 2 (BCL2) and myeloid cell leukemia sequence 1 (MCL1) were also compared between transfected and wild‑type HLE‑B3 cells by western blot analysis. The results showed that transfection with the miR‑15a‑3p mimic significantly suppressed the proliferation of HLE‑B3 cells, induced cell apoptosis and increased the proportion of early apoptotic cells. The migration of HLE‑B3 cells was significantly inhibited following transfection with miR‑15a‑3p mimic (P<0.01), whereas cell invasion was unaffected (P>0.05). In addition, reduced protein levels of BCL2 and MCL1 were observed in the miR‑15a‑3p mimic‑transfected HLE‑B3 cells (P<0.01). In conclusion, miR‑15a‑3p may suppress cell proliferation and migration, and induce cell apoptosis in lens epithelial cells through inhibiting the expression of BCL2 and MCL1, which contributes to the onset of ARCs.

Keywords: microRNA-15a; human lens epithelial cell; age-related cataract.

MeSH terms

  • Aged
  • Antagomirs / genetics
  • Antagomirs / metabolism
  • Apoptosis / genetics*
  • Cataract / genetics
  • Cataract / metabolism
  • Cataract / pathology
  • Cell Line, Transformed
  • Cell Movement
  • Cell Proliferation
  • Epithelial Cells / metabolism
  • Epithelial Cells / pathology
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Lens, Crystalline / metabolism*
  • Lens, Crystalline / pathology
  • MicroRNAs / agonists
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Models, Biological
  • Myeloid Cell Leukemia Sequence 1 Protein / genetics*
  • Myeloid Cell Leukemia Sequence 1 Protein / metabolism
  • Oligoribonucleotides / genetics
  • Oligoribonucleotides / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / genetics*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction
  • Transfection

Substances

  • Antagomirs
  • BCL2 protein, human
  • MCL1 protein, human
  • MIRN15 microRNA, human
  • MicroRNAs
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Oligoribonucleotides
  • Proto-Oncogene Proteins c-bcl-2