ArticleBMC molecular and cell biology2021
Increased expression of MUSASHI1 in epithelial breast cancer cells is due to down regulation of miR-125b.
Article in BMC molecular and cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Tumor suppressor effects of miR-143 and miR-199 on the K562 myelogenous leukemia cell line by targeting the RNA-binding protein Musashi2.Scientific reports · 2026Article
- Largazole targets Musashi protein expression via miR-125b-5p and sensitizes triple-negative breast cancer cells to radiation.Frontiers in pharmacology · 2026Article
- The Musashi RNA-binding proteins in female cancers: insights on molecular mechanisms and therapeutic relevance.Biomarker research · 2023Review
- Dysfunction and ceRNA network of the tumor suppressor miR-637 in cancer development and prognosis.Biomarker research · 2022Review
- Regulatory mechanisms and potential medical applications of HNF1A-AS1 in cancers.American journal of translational research · 2022Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMusashi1 (MSI1) is an oncogenic protein with a crucial role in the proliferation and characteristics of the epithelial cells in breast cancer. The change in expression of MSI1 has a role in solid tumor progression. There are different factors that regulate MSI1 expression in various cancer tissues including microRNAs which are considered as one of the most important of these factors. The aim of our study is identification of the molecular cause of maximal expression of MSI1 in epithelial breast cancer cell lines.
resultsAmong predicted microRNAs, miR-125b, miR-637 and miR-802 were able to significantly reduce the luciferase activity. In addition, the relative expression of these three miRNAs were measured in the cancerous cell lines that results showed a significant reduction in expression of all microRNAs. On the other hand, only the overexpression of miR-125b caused a change in the expression pattern of MSI1 in breast epithelial cancer cell lines. Accordingly, our results demonstrated that the exogenous expression of miR-125b decreased not only the MSI1 protein but also expression of epithelial markers in breast cancer cells.
conclusionsThe results of luciferase reporter assay showed that MSI1 is a direct target for miR-125b in epithelial breast cancer cells. Moreover, higher amount of MSI1 in those cell lines seems due to the reduced amount of miR-125b, which is responsible for epithelial features of those kinds of cancer cells. Therefore, the modulation of miR-125b may be a potential approach to help to combat against epithelial breast tumors.
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