Analysis of Chromosome 17 miRNAs and Their Importance in Medulloblastomas

López-Ochoa, Sebastian; Ramirez-Garcia, M. A.; Castro-Sierra, Eduardo; Arenas-Huertero, Francisco

doi:10.1155/2015/717509

Cited by 8 publications

(5 citation statements)

References 51 publications

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“…For example, 8 SDE-circRNA were all derived from chromosome 17, with nearly half of the genes with upregulated expression (46%, 6 out of 13) distributed on this chromosome ( Figure 1 B). Given that chromosome 17 is associated with many cancers [ 23 , 24 , 25 ], therefore, it is also worth exploring the circRNA related to cancer from chromosome 17.…”

Section: Resultsmentioning

confidence: 99%

Hsa_circ_0044301 Regulates Gastric Cancer Cell’s Proliferation, Migration, and Invasion by Modulating the Hsa-miR-188-5p/DAXX Axis and MAPK Pathway

Jiang

Liu

Chen

et al. 2022

Cancers

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Background: Despite advances in diagnostic and therapeutic technologies, the prognosis of patients with gastric cancer (GC) remains poor, necessitating further search for more effective therapeutic targets and markers for prognosis prediction. Circular RNA (circRNA) plays a role in various diseases, including GC. Methods: CircRNA expression in GC tissues was detected by circRNA microarray and quantitative reverse transcription polymerase chain reaction (qRT-PCR). The correlation between circRNA-0044301 and patient survival was analyzed by log-rank test and Cox regression analysis. Next, in vitro characterization and functional analysis of circRNA-0044301 was done by various assays using RNase R, actinomycin D, and RNA fluorescence in situ hybridization, as well as investigations into its use as a drug to treat tumors in a subcutaneous tumorigenesis model. RNA immunoprecipitation and dual-luciferase reporter assays were used to identify circRNA-0044301-related miRNA (miRNA-188-5p), key proteins of the related pathway (ERK1/2), and the downstream target DAXX. Finally, we investigated the relationship between circRNA-0044301 and ravoxertinib (GDC-0994) and 5-fluorouracil (5-FU) using qRT-PCR, Western blotting, and CCK8 assays. Results: CircRNA-0044301 was upregulated in tissues and cancer cells compared to its levels in controls, related to patient prognosis, and its specific siRNA-vivo could slow tumor growth. On the mechanism, it acted as a sponge of miRNA-188-5p, could regulate the downstream target DAXX, and modulated the effect of GDC-0994 on ERK1/2 and 5-FU in cells. Conclusions: CircRNA-0044301/miRNA-188-5p/DAXX (ERK1/2) may be a key axis in GC progression, and circRNA-0044301 has immense potential to be a therapeutic target for GC.

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Section: Resultsmentioning

confidence: 99%

Hsa_circ_0044301 Regulates Gastric Cancer Cell’s Proliferation, Migration, and Invasion by Modulating the Hsa-miR-188-5p/DAXX Axis and MAPK Pathway

Jiang

Liu

Chen

et al. 2022

Cancers

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“…miR-424 is a breast cancer suppressor, and loss of miR-424 expression can enhance resistance to chemotherapy ( 23 , 24 ). Thus, they not only could be specific diagnostic markers for certain malignant tumors and hereditary diseases, but also indicators of invasion, migration, drug resistance or prognosis of malignant tumors ( 26 , 27 ). A previous study analyzed the results of a glioma-related GeneChip and found that there are ~22 differentially expressed miRNAs, and that some miRNAs promote the proliferation of GBM cells ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑181a‑5p inhibits the proliferation and invasion of drug‑resistant glioblastoma cells by targeting F‑box protein 11 expression

Wen

Guo

et al. 2020

Oncol Lett

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Glioblastoma (GBM) is the most common malignant primary tumor in the human central nervous system. The present study aimed to explore the molecular mechanism by which microRNA (miR)-181a-5p targets the F-box protein 11 (FBXO11) in glioma cells to inhibit cell proliferation and invasion. Reverse transcription-quantitative (RT-q)PCR was performed to detect the expression levels of miR-181a-5p in U251TR cells, U251 cells, primary GBM tissues and relapsed GBM tissues in order to determine the association between miR-181a-5p and the chemoresistance of GBM cells. The expression levels of miR-181a-5p in GBM cells were modulated via transfecting miR-181a-5p mimics and inhibitors. Cell Counting Kit-8 assays were undertaken to assess the effects of miR-181a-5p on drug sensitivity and proliferation of GBM cells. Wound healing assays were performed to examine the effects of miR-181a-5p on the migratory ability of GBM cells. Furthermore, the effects of miR-181a-5p on the invasive ability of GBM cells were analyzed using an in vitro invasion assay. Flow cytometry analysis was carried out to determine whether overexpression of miR-181a-5p can promote the apoptotic rate of GBM cells. RT-qPCR and western blotting were employed to detect the effects of miR-181a-5p on mRNA and protein expression of FBX011. miR-181a-5p exhibited low expression in resistant GBM cell lines and recurrent tumor tissues. Dual-luciferase reporter assays were utilized to detect luciferase activity to verify the targeted regulatory association between miR-181a-5p and FBXO11. Upregulation of miR-181a-5p promoted the sensitivity of GBM cells to temozolomide (TMZ), increased the apoptotic rate of GBM cells and significantly inhibited the invasive and migratory capacities of GBM cells. In drug-resistant glioma cells, compared with the miR-negative control group and the blank group, the expression of miR-181a-5p was significantly upregulated (P<0.01), while the expression of FBXO11 protein was downregulated. miR-181a-5p increased the sensitivity of GBM cells to TMZ. miR-181a-5p significantly inhibited the migratory and invasive capacities of GBM cells. miR-181a-5p may become a novel effective target for the treatment of GBM. The results of dual-luciferase reporter assays indicated that miR-181a-5p could target the 3'-untranslated region of FBXO11. The underlying mechanism may be targeted inhibition of FBXO11 gene expression, or may be associated with apoptosis.

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“…The recent studies have demonstrated that several micro-RNAs (miRNAs) are associated with the invasion process in gliomas and other tumor cells. 10,11 MicroRNAs are highly conserved endogenous small noncoding RNAs, which contain 19 to 21 nucleotides and suppress gene expression posttranscriptionally by targeting the 3 0 untranslated regions of messenger RNAs (mRNAs). 12 MicroRNAs have gained more attention in regulating molecular pathogenesis of cancer recently, because each miRNA could suppress hundreds of targets that may play various roles in different tissues or cells.…”

Section: Introductionmentioning

confidence: 99%

miR-139 Functions as An Antioncomir to Repress Glioma Progression Through Targeting IGF-1 R, AMY-1, and PGC-1β

Wang

Yan²,

et al. 2016

Technol Cancer Res Treat

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Gliomas are the most common primary malignant brain tumor with poor prognosis, characterized by a highly heterogeneous cell population, extensive proliferation, and migration. A lot of molecular mechanisms regulate gliomas development and invasion, including abnormal expression of oncogenes and variation of epigenetic modification. MicroRNAs could affect cell growth and functions. Several reports have demonstrated that miR-139 plays multifunctions in kinds of solid tumors through different pathways. However, the antitumor mechanisms of this miR-139 are not unveiled in detail. In this study, we not only validated the low expression level of miR-139 in glioma tissues and cell lines but also detected the effect of miR-139 on modulating gliomas proliferation and invasion both in vitro and in vivo. We identified insulin-like growth factor 1 receptor, associate of Myc 1, and peroxisome proliferator-activated receptor γ coactivator 1β as direct targets of miR-139 and the levels of them were all inversely correlated with miR-139 in gliomas. Insulin like growth factor 1 receptor promoted gliomas invasion through Akt signaling and increased proliferation in the peroxisome proliferator-activated receptor γ coactivator 1β-dependent way. Associate of Myc 1 also facilitated gliomas progression by activating c-Myc pathway. Overexpression of the target genes could retrieve the antitumor function of miR-139, respectively, in different degrees. The nude mice transplantation tumor experiment displayed that glioma cells stably expressed miR-139 growth much slower in vivo than the negative control cells. Taken together, these findings suggested miR-139 acted as a favorable factor against gliomas progression and uncovered a novel regulatory mechanism, which may provide a new evidenced prognostic marker and therapeutic target for gliomas.

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Analysis of Chromosome 17 miRNAs and Their Importance in Medulloblastomas

Cited by 8 publications

References 51 publications

Hsa_circ_0044301 Regulates Gastric Cancer Cell’s Proliferation, Migration, and Invasion by Modulating the Hsa-miR-188-5p/DAXX Axis and MAPK Pathway

Hsa_circ_0044301 Regulates Gastric Cancer Cell’s Proliferation, Migration, and Invasion by Modulating the Hsa-miR-188-5p/DAXX Axis and MAPK Pathway

miR‑181a‑5p inhibits the proliferation and invasion of drug‑resistant glioblastoma cells by targeting F‑box protein 11 expression

miR-139 Functions as An Antioncomir to Repress Glioma Progression Through Targeting IGF-1 R, AMY-1, and PGC-1β

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