Circ_0021350 plays an oncogene role by regulating miR-1207-3p/ PIK3R3 in glioblastoma
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE222421 | GEO | 2024/01/10
REPOSITORIES: GEO
Similar Datasets
Project description:BackgroundGlioblastoma (GBM) is the most malignant glioma, with poor survival rates and prognosis. Several studies have reported the abnormal expression of circular RNAs (circRNAs) and their functions in the malignant biological behavior of GBM. However, such research is still in the preliminary stages, and further study is needed to confirm the therapeutic potential of circRNAs in GBM.MethodsRNA-seq was performed using four tumor tissues from patients with GBM and their adjacent non-tumor brain tissues to screen differentially expressed circRNAs. Fluorescence in situ hybridization assay was used to examine the location of circ_0021350 in glioma cells. In addition, a series of biological function assays were employed to verify the oncogenic role of circ_0021350 in GBM. Quantitative reverse transcription PCR was used to examine circular, micro- (miRNA), and messenger RNA (mRNA) levels. Furthermore, dual-luciferase reporter, RNA pull-down, and RNA binding protein immunoprecipitation assays were applied to verify the interaction between circ_0021350 and its downstream effectors.ResultsCirc_0021350 was significantly elevated in GBM tissues and glioma cells. Overexpression of circ_0021350 promoted glioma cell proliferation and metastatic ability; silencing of circ_0021350 had the opposite effect. Mechanistic analysis revealed that circ_0021350 sponged miR-1207-3p to regulate PIK3R3, whose overexpression reversed the reduction in the malignant biological behavior of glioma cells caused by silencing circ_0021350.ConclusionOur findings suggest that circ_0021350 is an oncogenic circRNA in GBM, and the circ_0021350/miR-1207-3p/PIK3R3 axis may serve as a potential therapeutic target in GBM treatment.
| S-EPMC10463850 | biostudies-literature
Project description:Circ_0021350 plays an oncogene role by regulating miR-1207-3p/ PIK3R3 in glioblastoma
| PRJNA922055 | ENA
Project description:BackgroundMultiple myeloma remains a virtually incurable hematologic malignancy, which is featured with the aberrant growth of malignant plasma cells.AimsTo elucidate the functions of miR-19a-3p in multiple myeloma.Study designCell study.MethodsCell counting kit-8 assay was performed to detect cell viability, and flow cytometry was conducted to detect cell apoptosis. Bioinformatics analysis predicted miR-19a-3p-associated biological function, pathway, core regulatory network, and target genes. Luciferase reporter assay verified the target sequence of miR-19a-3p regulating FBXO32.ResultsmiR-19a-3p is upregulated in multiple myeloma cells (p<0.01) and patients with multiple myeloma (p<0.001). Overexpressed miR-19a-3p significantly increased cell viability (p<0.05) and inhibited cell apoptosis (p<0.01). FBXO32 is a target gene of miR-19a-3p (p<0.01). Moreover, FBXO32 is downregulated in MM, and it significantly decreased cell viability (p<0.05) and promoted cell apoptosis (p<0.01). FBXO32 significantly rescued the influence of miR-19a-3p-inhibiting cell apoptosis (p<0.05).ConclusionmiR-19a-3p promoted cell proliferation and inhibited cell apoptosis by degrading the target FBXO32 mRNA in multiple myeloma.
| S-EPMC8909224 | biostudies-literature
Project description:We used microarrays to perform systematic profiling of human microRNAs in serum from glioblastoma multiforme (GBM) patients to find potential biomarkers. By comparing the serum microRNA profiles of the GBM patients and healthy volunteers, potential biomarkers for GBM were investigated. Using a custom microarray platforms containing 1843 species of miRNAs, we previously identified 19 serum miRNAs with differential expression in GBM patients.
2017-11-01 | GSE93850 | GEO
Project description:Background: The hypoxia microenvironment is highly associated with GBM’s malignant phenotypes. CircRNAs were reported involved in GBM’s biological characteristics and regulated by HIF-1α. However, the differential expression profile and role of circRNAs in GBM cells under hypoxia are still unclear. Methods: The expression profiles of circRNAs in LN229 and T98G under hypoxia were explored via circRNA sequencing analysis. Those circRNAs significantly dysregulated both in LN229 and T98G, and could be found in circBase were selected and validated by qRT-PCR, RNase R digestion reaction and Sanger sequencing. Normal cell line and fresh GBM tissues were also used for qRT-PCR validation. The roles of differentially expressed circRNAs were evaluated by bioinformatics analyses. Results: There were 672 dysregulated circRNAs in LN229 and 698 dysregulated circRNAs in T98G. GO analysis indicated that the alteration of circRNAs expression related to GBM cell’s biogenesis and metabolism. KEGG analysis demonstrated that TGF-β signaling pathway, HIF-1 signaling pathway and metabolism related signaling pathway were closely associated with differentially expressed circRNAs under hypoxia. The 6 selected and dysregulated circRNAs both in LN229 and T98G including hsa_circ_0000745, hsa_circ_0020093, hsa_circ_0020094, hsa_circ_0000943, hsa_circ_0004874 and hsa_circ_0002359 were validated by qRT-PCR. HIF-1α centered circRNA-miRNA-mRNA networks analysis showed that the 6 validated circRNAs could cross-talk with 11 related miRNAs. Conclusion: The circRNA expressions are dysregulated in GBM cell under hypoxia. The 6 validated circRNAs could participate in GBM’s development and progression when hypoxia occurs. They might be the candidates for prognostic markers and adjuvant therapeutics of GBM in the future.
2024-12-28 | GSE192678 | GEO
Project description:This microarray contains expression data for two GBM tissue samples, four GSC cultures grown as spheres and one NFC culture grown as spheres Total RNA was isolated from GSC cultures and GBM tissues
2015-11-26 | E-GEOD-60705 | biostudies-arrayexpress
Project description:Arsenic resistance protein 2 (Ars2) is a component of the nuclear RNA cap-binding complex (CBC) that is important for some microRNA biogenesis and it is critical for cell proliferation and tumorigenicity. However, mechanism of Ars2-regulated cellular proliferation and tumorigenicity in glioblastoma has not been fully understood. Western blotting was used to detect the expressions of Ars2, p53, p21, and cleavage/activation of caspases-3 (C-Caspase 3). Microarray and Quantitative Real-time PCR (qRT-PCR) were performed to identify the Ars2-regulated microRNAs. Apoptosis assessed by flow cytometry analysis was used to evaluate the role of Ars2 in cells proliferation. The lentivirus-mediated gene knockdown approach was conducted to determine the function of Ars2. The orthotopic glioblastoma xenograft was used to demonstrate the role of Ars2 in glioblastoma growth in vivo. The high expression of Ars2 was observed in several glioblastoma cell lines and was significantly associated with poorer overall survival. Importantly, the overexpression of Ars2 promoted cell proliferation and colony formation in glioblastoma cells, whereas the depletion of Ars2 inhibited cell proliferation, colony formation, and tumor growth. Mechanistic study revealed that knockdown of Ars2 reduced the expression levels of miR-6798-3p, which was responsible for the up-regulation of p53 and p21, leading to apoptosis. Furthermore, the knockdown of Ars2 suppressed tumor growth in orthotopic glioblastoma xenograft model and significantly prolonged the survival time of the tumor-bearing mice. These findings identify a critical role for Ars2 in regulation of proliferation and tumorigenicity in glioblastoma and suggest that Ars2 could be a critical therapeutic target for glioblastoma intervention.
| S-EPMC6197286 | biostudies-literature
Project description:Glioblastoma (GBM) is one of the most common and malignant types of primary cancer in the central nervous system; however, the clinical outcomes of patients with GBM remain poor. Circular RNAs (circRNAs) have been revealed to serve important roles in diverse biological processes, such as regulating cell proliferation, epithelial‑mesenchymal transition and tumor development. However, the underlying biological function of circRNA filamin A (circFLNA) and its potential role in GBM remain to be determined. The present study aimed to identify differentially expressed circRNAs in GBM. Reverse transcription‑quantitative PCR was used to analyze the expression levels of circFLNA. The results demonstrated that the expression levels of circFLNA were significantly upregulated in clinical GBM samples and GBM cells compared with adjacent healthy brain tissues and normal human astrocytes, respectively. The results of the Cell Counting Kit‑8 and Transwell assays revealed that circFLNA knockdown significantly inhibited the proliferative and invasive abilities of GBM cell lines. Moreover, high circFLNA expression levels were associated with a worse prognosis in GBM. MicroRNA (miR)‑199‑3p was subsequently predicted to be target of circFLNA. The inhibitory effect of miR‑199‑3p on cell proliferation and invasion was partially reversed following circFLNA knockdown. In conclusion, the findings of the present study identified novel roles for circFLNA in GBM and indicated that the circFLNA/miR‑199‑3p signaling axis may serve an important role in GBM progression. Therefore, circFLNA may represent a novel target for the diagnosis and treatment of GBM.
| S-EPMC8441964 | biostudies-literature
Project description:Purpose:Long non-coding RNAs have been found to be involved in bladder cancer development. This article studied LINC00963 effects on bladder cancer progression to provide a novel treatment target. Patients and Methods:Totally 56 bladder cancer patients participated in this research. Bladder cancer cells were transfected. Cell counting kit 8 assay and clone formation experiment were used for cell viability and colony formation detection. Cell migration and invasion were determined by Transwell experiment. LINC00963 distribution was explored by cytoplasmic and nuclear extract isolation and quantitative real-time polymerase chain reaction. Luciferase reporter experiment and RNA pulldown experiment were performed to detect the relationship between these two genes. The cancer genome atlas analysis was used for the detection of metastasis-associated protein 1 (MTA1) expression in bladder cancer. Results:LINC00963 was seriously up-regulated in bladder cancer patients. High LINC00963 expression indicated high histological grade and low survival. LINC00963 was obviously up-regulated in bladder cancer cells. Knockdown of LINC00963 significantly reduced bladder cancer cells viability, colony formation, migration and invasion. Luciferase reporter experiment and RNA pulldown experiment revealed that LINC00963 promoted MTA1 expression via directly inhibiting miR-766-3p. MTA1 was up-regulated in bladder cancer patients. MTA1 up-regulation reversed the inhibitory effect of LINC00963 knockdown on bladder cancer cell viability, migration and invasion. Conclusion:LINC00963 functions as an oncogene in bladder cancer by regulating the miR-766-3p/MTA1 axis.
| S-EPMC7229805 | biostudies-literature
Project description:Glioblastoma (GBM) is characterized by aggressive invasiveness, with the role of circular RNAs (circRNAs) in this process remains unknown. Here, we identify circMETTL3 as a key regulator of GBM invasion through analyzing the core and invasive margin cells from patient samples and animal models. circMETTL3 is significantly upregulated in GBM tumors compared to normal tissues and enhances invasiveness in vitro and in vivo. Mechanistically, circMETTL3 selectively binds to the 5'UTR of invasion-related mRNAs, such as ADAMTS5 (a disintegrin and metalloproteinase with thrombospondin motifs 5), promoting ADAMTS5 translation in a Y-box-binding protein 1 (YBX1)-dependent manner, thereby driving GBM migration and invasion. Furthermore, elevated circMETTL3 correlates with higher ADAMTS5 expression, increased GBM invasion and poor survival of GBM patients. Therefore, these findings highlight the substantial role of circMETTL3 in accelerating GBM malignancy through regulating translation of certain mRNAs, underscoring its potential as a prospective biomarker and therapeutic target for GBM.
2025-01-20 | PXD059996 |