Up-Regulated Expression of miR-23a/b Targeted the Pro-Apoptotic Fas in Radiation-Induced thymic Lymphoma
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BACKGROUND: MicroRNAs (miRNAs) are small, single-stranded, noncoding RNAs, which usually bind to the 3'-untranslated region of target mRNAs and are capable of inducing posttranscriptional gene regulation by blocking translation or by degrading the target mRNA. However, the expression level of miR-23 in radiation induced carcinogenesis is largely unknown. METHODS: Radiation induced thymic lymphoma model in BALB/c mice was set up. miR-23a & miR-23b miRNA levels in different tissues and cells were detected by real-time qPCR. miR-23a/b inhibitor and miR-23a/b mimics were transfected to lymphoma cells and the target of miR-23a/b was identified by microRNA target prediction and Luciferase assays. RESULTS: We found that miR-23a & miR-23b were up-regulated in radiation induced thymic lymphoma tissue samples. Cell death and apoptosis were increased by miR-23a/b inhibitor and decreased by miR-23a/b mimics in lymphoma cells. Computational analysis found a putative target site of miR-23a/b in the 3'UTR of Fas mRNA, which was verified by luciferase reporter assay. Forced over-expression of miR-23a/b decreased the level of Fas protein. Moreover, over-expression of Fas rescued the pro-proliferation effect of miR-23, indicating Fas is a direct mediator of miR-23 functions. Furthermore, contrast to miR-23a/b which was up regulated, the Fas expression level was down-regulated and inversely correlated with miR-23 in split radiation induced lymphoma tissue samples. Finally, our data also indicates that miR-23a could repress Fas much more potent than miR-23b and the additional region besides conserved seed pairing enables miR-23a's higher regulation. CONCLUSIONS: In this study, using a radiation induced thymic lymphoma model in BALB/c mice, We conclude that the expression of miR-23a/b is up-regulated in radiation-induced thymic lymphoma and it maybe a novel therapeutic target of that cancer.
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Unlike the functional differentiation of miR-23a/miR-23b in ovarian cancer, their expression levels are upregulated in radiation-induced thymic lymphoma model mice and share a common target gene Fas.
“Unlike the functional differentiation of miR-23a/miR-23b in OC, their expression levels are upregulated in radiation-induced thymic lymphoma model mice and share a common target gene Fas.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [96]
Treatment by inhibitors of miR-23a/miR-23b can both boost cell death and apoptosis in lymphoma cells.
“Treatment by inhibitors of miR-23a/miR-23b can both boost cell death and apoptosis in lymphoma cells [96].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [96]
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- Authors
- Li, B., Sun, M., Gao, F., Liu, W., Yang, Y., Liu, H., Cheng, Y., Liu, C., & Cai, J.
- Affiliations
- Second Military Medical University (CN)
- Venue
- Cellular Physiology and Biochemistry
- Publisher
- S. Karger AG
- Published
- 2013
- Volume
- 32
- Issue
- 6
- Pages
- 1729-1740
- ISSN
- 1015-8987 (ISSN-L)
- 1421-9778
- OpenAlex
- W2036859638
- Cited by
- 54
- References
- 55
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 4 · 2019: 6 · 2018: 6 · 2017: 5 · 2016: 9 · 2015: 8 · 2014: 5
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cellular Physiology and Biochemistry (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (31100605, 31070761)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- miR-23a, miR-23b, microRNA, Fas, radiation-induced thymic lymphoma, apoptosis, 3' untranslated region, post-transcriptional regulation, radiation-induced cancer
- MeSH terms
- Animals, Base Sequence, Binding Sites, Lymphoma, Mice, Inbred BALB C, Radiation, Ionizing, Thymus Neoplasms, Down-Regulation, Up-Regulation, Oligonucleotides, Antisense, Sequence Alignment, Apoptosis, fas Receptor, 3' Untranslated Regions, MicroRNAs, NIH 3T3 Cells, Cell Line, Tumor, Cell Proliferation, Mice
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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