ArticleAmerican journal of cancer research2017
MicroRNA-1179 inhibits glioblastoma cell proliferation and cell cycle progression via directly targeting E2F transcription factor 5.
Article in American journal of cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- New Insights into the Development of Papillary Thyroid Cancer: The Roles of miR-1179 and ELF3.Cells · 2026Article
- Article
- A Review of the Regulatory Mechanisms of N-Myc on Cell Cycle.Molecules (Basel, Switzerland) · 2023Review
- Underlying mechanisms and clinical potential of circRNAs in glioblastoma.Oncology research · 2023Review
- CircFOXM1 promotes the proliferation, migration, invasion, and glutaminolysis of glioblastoma by regulating the miR-577/E2F5 axis.Bosnian journal of basic medical sciences · 2022Article
- MiR-1179 represses cell proliferation, migration and invasion of hepatocellular carcinoma through suppression of NUAK2.American journal of translational research · 2022Article
- CircFOXM1 promotes proliferation and metastasis of hepatocellular carcinoma via regulating miR-1179/SPAG5 axis.Scientific reports · 2021Article
- CircRFX3 contributes to glioma progression through the circRFX3-miR-1179/miR-1229-VASP axis.Cancer cell international · 2021Article
- miR-720 is a key regulator of glioma migration and invasion by controlling TARSL2 expression.Human cell · 2021Article
- Article
- Overview of host miRNA properties and their association with epigenetics, long non-coding RNAs, and Xeno-infectious factors.Cell & bioscience · 2021Review
- Overexpression of microRNA-129-5p in glioblastoma inhibits cell proliferation, migration, and colony-forming ability by targeting ZFP36L1.Bosnian journal of basic medical sciences · 2020Article
- Comprehensive analysis of a long non-coding RNA-associated competing endogenous RNA network in glioma.Oncology letters · 2020Article
- Article
- Long non-coding RNA NPBWR1-2 affects the development of ovarian cancer via multiple microRNAs.Oncology letters · 2020Article
- LncRNA SNHG5 promotes nasopharyngeal carcinoma progression by regulating miR-1179/HMGB3 axis.BMC cancer · 2020Article
- miR-210-5p promotes epithelial-mesenchymal transition by inhibiting PIK3R5 thereby activating oncogenic autophagy in osteosarcoma cells.Cell death & disease · 2020Article
- miR-525-5p Modulates Proliferation and Epithelial-Mesenchymal Transition of Glioma by Targeting Stat-1.OncoTargets and therapy · 2020Article
- Expression, Prognosis, and Immune Infiltrates Analyses of E2Fs in Human Brain and CNS Cancer.BioMed research international · 2020Article
- CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2.Cancer cell international · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is an extraordinary aggressive disease that requires more effective therapeutic options. In the past few years, many microRNAs (miRNAs) have been demonstrated to have important roles in promoting GBM progression. However, little is known about the role of miR-1179 in GBM. In the present study, we found that miR-1179 was significantly downregulated in glioma tissues and cell lines. Functional experiments showed that introduction of miR-1179 dramatically suppressed GBM cell proliferation and cell cycle progression. Importantly, treatment of miR-1179 strongly inhibited tumor growth in a subcutaneous GBM model. Further studies showed that E2F transcription factor 5 (E2F5), a key transcription factor that controls cell cycle transition, was a direct target of miR-1179. Silencing of E2F5 inhibited the proliferative ability of GBM cells and induces cell cycle arrest, which were consistent with the effects of miR-1179 overexpression. More importantly, reintroduction of E2F5 into GBM cells reversed the tumor-suppressive function of miR-1179. Finally, we demonstrated that miR-1179 expression was negatively correlated with E2F5 messenger RNA (mRNA) levels in high-grade gliomas. Our findings provide new insights into the role of miR-1179 in the progression of GBM, and implicate the potential application of miR-1179 in GBM therapy.
Indexed as
Identifiers
28861324PMC5574940W3023166814What 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.