ArticleMedical science monitor : international medical journal of experimental and clinical research2016
Down-Regulation of MicroRNA-133b Suppresses Apoptosis of Lens Epithelial Cell by Up-Regulating BCL2L2 in Age-Related Cataracts.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Suppression of miR-195 attenuates oxygen-glucose deprivation/reperfusion-induced BBB destruction, possibly via targeting BCL2L2.Frontiers in neuroscience · 2026Article
- Aging of the human eye lens: Epigenetic landscape and therapeutic targets in age‑related cataracts (Review).International journal of molecular medicine · 2025Review
- Let-7c-3p suppresses lens epithelial-mesenchymal transition by inhibiting cadherin-11 expression in fibrotic cataract.Molecular and cellular biochemistry · 2024Article
- Knockdown of lncRNA TUG1 protects lens epithelial cells from oxidative stress-induced injury by regulating miR-196a-5p expression in age-related cataracts.Experimental and therapeutic medicine · 2021Article
- Effects of microRNA-195 on the Prognosis of Glioma Patients and the Proliferation and Apoptosis of Human Glioma Cells.Pathology oncology research : POR · 2020Article
- Let-7c-3p Regulates Autophagy under Oxidative Stress by Targeting ATG3 in Lens Epithelial Cells.BioMed research international · 2020Article
- lncRNA H19 contributes to oxidative damage repair in the early age-related cataract by regulating miR-29a/TDG axis.Journal of cellular and molecular medicine · 2019Article
- miR‑15a‑3p affects the proliferation, migration and apoptosis of lens epithelial cells.Molecular medicine reports · 2019Article
- miR-422a inhibits osteosarcoma proliferation by targeting BCL2L2 and KRAS.Bioscience reports · 2018Article
- miR-24-p53 pathway evoked by oxidative stress promotes lens epithelial cell apoptosis in age-related cataracts.Molecular medicine reports · 2018Article
- miR-211 regulates the antioxidant function of lens epithelial cells affected by age-related cataracts.International journal of ophthalmology · 2018Article
- miR-211 promotes lens epithelial cells apoptosis by targeting silent mating-type information regulation 2 homolog 1 in age-related cataracts.International journal of ophthalmology · 2018Article
- IFN-γ-induced microRNA-29b up-regulation contributes tokeratinocyte apoptosis in atopic dermatitis through inhibiting Bcl2L2.International journal of clinical and experimental pathology · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND MicroRNA-133b (miR-133b) has been reported to be involved in many diseases, including ovarian cancer and osteosarcoma. Accumulating evidence suggests that miR-133b plays important roles in human disease. In this study, we aimed to investigate the molecular mechanism, including the potential regulator and signaling pathways, of BCL2L2. MATERIAL AND METHODS We first searched the online miRNA database (www.mirdb.org) using the "seed sequence" located within the 3'-UTR of the target gene, and then performed luciferase assay to test the regulatory relationship between miR-133b and BCL2L2. Western blot and real-time PCR were used to determine the expression of BCL2L2 in human samples or cells treated with miRNA mimics or inhibitors. Flow cytometry was conducted to evaluate the apoptosis status of the cells. RESULTS We validated BCL2L2 to be the direct gene using a luciferase reporter assay. We also conducted real-time PCR and Western blot analyses to study the mRNA and protein expression level of BCL2L2 among different groups (control: n=29, cataract: n=33) or cells treated with scramble control, miR-133b mimics, BCL2L2 siRNA, and miR-133b inhibitors, and identified the negative regulatory relationship between miR-133b and BCL2L2. We also conducted experiments to investigate the influence of miR-133b and BCL2L2 on the viability and apoptosis of cells. The results showed that miR-133b positively interfered with the viability of cells, while BCL2L2 negatively interfered with the viability of cells, and that miR-133b inhibited apoptosis while BCL2L2 accelerated apoptosis. CONCLUSIONS BCL2L2 was the virtual target of miR-133b, and we found a negative regulatory relationship between miR-133b and BCL2L2. MiR-133b and BCL2L2 interfered with the viability and apoptosis of cells.
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