ArticleInternational journal of cancer2015
Expression of the miR-302/367 cluster in glioblastoma cells suppresses tumorigenic gene expression patterns and abolishes transformation related phenotypes.
Article in International journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Role of noncoding RNA as a pacemaker in cancer stem cell regulation: a review article.Journal of the Egyptian National Cancer Institute · 2025Review
- Emerging Insights into the PI3K/AKT/mTOR Signaling Pathway and Non-Coding RNA-mediated Drug Resistance in Glioblastoma.Current molecular medicine · 2025Review
- KLF4 is an epigenetically modulated, context-dependent tumor suppressor.Frontiers in cell and developmental biology · 2024Review
- Review
- Expression Profile of mRNAs and miRNAs Related to the Oxidative-Stress Phenomenon in the Ishikawa Cell Line Treated Either Cisplatin or Salinomycin.Biomedicines · 2022Article
- SALL Proteins; Common and Antagonistic Roles in Cancer.Cancers · 2021Review
- Noncoding RNAs involved in the STAT3 pathway in glioma.Cancer cell international · 2021Review
- MicroRNA302-367-PI3K-PTEN-AKT-mTORC1 pathway promotes the development of cardiac hypertrophy through controlling autophagy.In vitro cellular & developmental biology. Animal · 2020Article
- Repression of TGF-β Signaling in Breast Cancer Cells by miR-302/367 Cluster.Cell journal · 2020Article
- MicroRNA-302 inhibits cell migration and invasion in cervical cancer by targeting DCUN1D1.Experimental and therapeutic medicine · 2018Article
- MicroRNA expression profiles in non‑epithelial ovarian tumors.International journal of oncology · 2018Article
- MicroRNA-23a/24-2/27a as a potential diagnostic biomarker for cancer: A systematic review and meta-analysis.Molecular and clinical oncology · 2018Article
- Combinatorial ensemble miRNA target prediction of co-regulation networks with non-prediction data.Nucleic acids research · 2017Article
- Cell-based therapy using miR-302-367 expressing cells represses glioblastoma growth.Cell death & disease · 2017Article
- Inhibition of miR-302 Suppresses Hypoxia-Reoxygenation-Induced H9c2 Cardiomyocyte Death by Regulating Mcl-1 Expression.Oxidative medicine and cellular longevity · 2017Article
- MicroRNAs in glioblastoma multiforme pathogenesis and therapeutics.Cancer medicine · 2016Review
- The role of octamer binding transcription factors in glioblastoma multiforme.Biochimica et biophysica acta · 2016Review
- MiR-302a/b/c/d cooperatively sensitizes breast cancer cells to adriamycin via suppressing P-glycoprotein(P-gp) by targeting MAP/ERK kinase kinase 1 (MEKK1).Journal of experimental & clinical cancer research : CR · 2016Article
- Emerging targets for glioblastoma stem cell therapy.Journal of biomedical research · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular transformation is initiated by the activation of oncogenes and a closely associated developmental reprogramming of the epigenetic landscape. Transcription factors, regulators of chromatin states and microRNAs influence cell fates in development and stabilize the phenotypes of normal, differentiated cells and of cancer cells. The miR-302/367 cluster, predominantly expressed in human embryonic stem cells (hESs), can promote the cellular reprogramming of human and mouse cells and contribute to the generation of iPSC. We have used the epigenetic reprogramming potential of the miR-302/367 cluster to "de-program" tumor cells, that is, hift their gene expression pattern towards an alternative program associated with more benign cellular phenotypes. Induction of the miR-302/367 cluster in extensively mutated U87MG glioblastoma cells drastically suppressed the expression of transformation related proteins, for example, the reprogramming factors OCT3/4, SOX2, KLF4 and c-MYC, and the transcription factors POU3F2, SALL2 and OLIG2, required for the maintenance of glioblastoma stem-like tumor propagating cells. It also diminished PI3K/AKT and STAT3 signaling, impeded colony formation in soft agar and cell migration and suppressed pro-inflammatory cytokine secretion. At the same time, the miR-302/367 cluster restored the expression of neuronal markers of differentiation. Most notably, miR-302/367 cluster expressing cells lose their ability to form tumors and to establish liver metastasis in nude mice. The induction of the miR-302/367 cluster in U87MG glioblastoma cells suppresses the expression of multiple transformation related genes, abolishes the tumor and metastasis formation potential of these cells and can potentially become a new approach for cancer therapy.
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