ArticlePloS one2014
MiR-101 induces senescence and prevents apoptosis in the background of DNA damage in MCF7 cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026Review
- Altered microRNA profiles and associated pathways in canine mammary adenocarcinoma.Scientific reports · 2025Article
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- Comprehensive systems biology analysis of microRNA-101-3p regulatory network identifies crucial genes and pathways in hepatocellular carcinoma.Journal, genetic engineering & biotechnology · 2025Article
- miRNome Profiling Detects miR-101-3p and miR-142-5p as Putative Blood Biomarkers of Frailty Syndrome.Genes · 2022Article
- Berberine Inhibits the Expression of SCT through miR-214-3p Stimulation in Breast Cancer Cells.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- A germline HLTF mutation in familial MDS induces DNA damage accumulation through impaired PCNA polyubiquitination.Leukemia · 2019Article
- Potential microRNA-related targets in clearance pathways of amyloid-β: novel therapeutic approach for the treatment of Alzheimer's disease.Cell & bioscience · 2019Review
- Key nodes of a microRNA network associated with the integrated mesenchymal subtype of high-grade serous ovarian cancer.Chinese journal of cancer · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Moderately increased DNA damage due to the exogenous miR-101 (4 fold) over-expression in MCF7 cells was substantiated by an increase in the number of γ-H2AX foci, correlating with a simple-to-do Halo-assay. miR-101 induced mild/moderate DNA damage favoured senescence rather than apoptosis. An experimental support emanated from the induced mild/moderate DNA damage with 1 µM/5 µM etoposide in MCF7 cells, which resulted in an endogenous miR-101 over-expression (10/4 fold, respectively), followed by senescence. On the other hand, the severe DNA damage induced with 10 µM etoposide, resulted in a low (<1 fold) endogenous expression of miR-101 and an elevated percentage of apoptotic cells. Using bioinformatics tools along with in-vitro and in-vivo validations, miR-101 was found to target and downregulate the mRNA expression of UBE2N and SMARCA4, involved in DNA damage repair (DDR) pathways. Recovery of the expression of the two novel targets in anti-miR-101 transfection validated the results. We conclude that a threshold range of over-expressed miR-101, capable of inducing mild/moderate DNA damage, is sensed by cells to become senescent. The observation derives further support from in-silico protein-protein network analysis where the two novel targets showed their involvement in senescence pathway.
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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.