ArticleOncotarget2015
MiR-208a stimulates the cocktail of SOX2 and β-catenin to inhibit the let-7 induction of self-renewal repression of breast cancer stem cells and formed miR208a/let-7 feedback loop via LIN28 and DICER1.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 68 citations in OpenAlex.
- MicroRNAs and Alarmins in Cardio-Oncology: Biomarkers and Therapeutic Implications in Skin and Breast Cancer.International journal of molecular sciences · 2026Review
- Lin28/let-7 axis in breast cancer.Molecular biology reports · 2025Review
- Enhancement of TKI sensitivity in lung adenocarcinoma through m6A-dependent translational repression of Wnt signaling by circ-FBXW7.Molecular cancer · 2023Article
- The Intricate Interplay between Cancer Stem Cells and Oncogenic miRNAs in Breast Cancer Progression and Metastasis.Life (Basel, Switzerland) · 2023Review
- Let-7a suppresses Ewing sarcoma CSCs' malignant phenotype via forming a positive feedback circuit with STAT3 and lin28.Journal of bone oncology · 2021Article
- The immunotherapy candidate TNFSF4 may help the induction of a promising immunological response in breast carcinomas.Scientific reports · 2021Article
- LncRNAs and microRNAs as Essential Regulators of Stemness in Breast Cancer Stem Cells.Biomolecules · 2021Review
- Stem signatures associated antibodies yield early diagnosis and precise prognosis predication of patients with non-small cell lung cancer.Journal of cancer research and clinical oncology · 2021Article
- Deficiency of miR-208a Exacerbates CClHepatology communications · 2020Article
- A SNP of miR-146a is involved in bladder cancer relapse by affecting the function of bladder cancer stem cells via the miR-146a signallings.Journal of cellular and molecular medicine · 2020Article
- Noncoding RNAs: the shot callers in tumor immune escape.Signal transduction and targeted therapy · 2020Review
- Cancer stem-like cells with hybrid epithelial/mesenchymal phenotype leading the collective invasion.Cancer science · 2020Article
- A genetic variant rs13293512 in the promoter of let-7 is associated with an increased risk of breast cancer in Chinese women.Bioscience reports · 2019Article
- ACancer cell international · 2019Article
- H19 regulation of oestrogen induction of symmetric division is achieved by antagonizing Let-7c in breast cancer stem-like cells.Cell proliferation · 2019Article
- MYC and DNMT3A-mediated DNA methylation represses microRNA-200b in triple negative breast cancer.Journal of cellular and molecular medicine · 2018Article
- Breast cancer stem-like cells are sensitized to tamoxifen induction of self-renewal inhibition with enforced Let-7c dependent on Wnt blocking.International journal of molecular medicine · 2018Article
- Therapeutic potential of microRNAs for the treatment of renal fibrosis and CKD.Physiological genomics · 2018Review
- MiR-129 blocks estrogen induction of NOTCH signaling activity in breast cancer stem-like cells.Oncotarget · 2017Article
- Dynamic and Modularized MicroRNA Regulation and Its Implication in Human Cancers.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MiR-208a stimulates cardiomyocyte hypertrophy, fibrosis and β-MHC (β-myosin heavy chain) expression, being involved in cardiovascular diseases. Although miR-208a is known to play a role in cardiovascular diseases, its role in cancer and cancer stem cells (CSCs) remains uncertain. We identified an inverse relationship between miR-208a and let-7a in breast cancer specimens, and found that SOX2, β-catenin and LIN28 are highly expressed in patients with advanced breast cancer opposed to lesser grades. Further, we isolated ALDH1+ CSCs from ZR75-1 and MDA-MB-231 (MM-231) breast cancer cell lines to test the role of miR-208a in breast CSCs (BrCSCs). Our studies showed that overexpression of miR-208a in these cells strongly promoted the proportion of ALDH1+ BrCSCs and continuously stimulated the self-renewal ability of BrCSCs. By using siRNAs of SOX2 and/or β-catenin, we found that miR-208a increased LIN28 through stimulation of both SOX2 and β-catenin. The knockdown of either SOX2 or β-catenin only partially attenuated the functions of miR-208a. Let-7a expression was strongly inhibited in miR-208a overexpressed cancer cells, which was achieved by miR-208a induction of LIN28, and the restoration of let-7a significantly inhibited the miR-208a induction of the number of ALDH1+ cells, inhibiting the propagations of BrCSCs. In let-7a overexpressed ZR75-1 and MM-231 cells, DICER1 activity was significantly inhibited with decreased miR-208a. Let-7a failed to decrease miR-208a expression in ZR75-1 and MM-231 cells with DICER1 knockdown. Our research revealed the mechanisms through which miR-208a functioned in breast cancer and BrCSCs, and identified the miR-208a-SOX2/β-catenin-LIN28-let-7a-DICER1 regulatory feedback loop in regulations of stem cells renewal.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.