miR‑592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin‑dependent kinase 8

Liu, Ting; Meng, Jingjing; Zhang, Yu

doi:10.3892/mmr.2020.11392

Cited by 6 publications

(5 citation statements)

References 53 publications

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“…By absorbing hsa-mir-940, hsa_circ_0092339 targets C-MYC indirectly and plays an important role in castration-resistant prostate cancer [ 32 ]. It is reported that miR-592 enhances medullary thyroid cancer tumorigenesis through cyclin-dependent kinase 8 [ 33 ]. MiR-592 suppresses the malignant phenotypes of thyroid cancer through the regulation of lncRNA NEAT1 and downregulation of NOVA1 [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of m7G Methylation-Related miRNA Signature Associated with Survival and Immune Microenvironment Regulation in Uterine Corpus Endometrial Carcinoma

Chen

Sun

Hou

et al. 2022

BioMed Research International

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Background. N7-methylguanosine (m7G) has been implicated in the development of cancer. The role of m7G-related miRNAs in the survival prediction of UCEC patients has not been investigated. Current research was the first to construct an m7G-related miRNA model to accurately predict the survival of patients with uterine corpus endometrial carcinoma (UCEC) and to explore immune cell infiltration and immune activity in the tumor microenvironment. Methods. RNA-seq data and clinical information of UCEC patients were derived from The Cancer Genome Atlas (TCGA) database. Using the TargetScan online database, we predicted miRNAs linked to the m7G-related genes and identified miRNAs which were significantly associated with the survival in UCEC patients and constructed a risk scoring model. The TCGA-UCEC cases were scored according to the risk model, and the high- and low-risk groups were divided by the median risk value. Gene enrichment analysis and immune cell infiltration and immune function analysis were performed using “clusterProfiler” and “GSVA” packages in R. Results. The survival prediction model consisted of 9 miRNAs, namely, hsa-miR-1301, hsa-miR-940, hsa-miR-592, hsa-miR-3170, hsa-miR-876, hsa-miR-215, hsa-miR-934, hsa-miR-3920, and hsa-miR-216b. Survival of UCEC patients in the high-risk group was worse than that in the low-risk group ( p < 0.001 ). The receiver operating characteristic (ROC) curve showed that the model had good predictive performance, and the area under the curve was 0.800, 0.690, and 0.705 for 1-, 3-, and 5-year survival predictions, respectively. There were differences in the degree of immune cell infiltration and immune activity between the low-risk and high-risk groups. The expression levels of the identified differentially expressed genes correlated with the susceptibility to multiple anticancer drugs. Conclusions. The survival prediction model constructed based on 9 m7G-related miRNAs had good predictive performance.

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Section: Discussionmentioning

confidence: 99%

Identification of m7G Methylation-Related miRNA Signature Associated with Survival and Immune Microenvironment Regulation in Uterine Corpus Endometrial Carcinoma

Chen

Sun

Hou

et al. 2022

BioMed Research International

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“…Gao et al show that miR-592 suppresses glioma cell growth and invasive growth by targeting Rho-associated protein kinase (ROCK1) [ 10 ]. In 2020, Liu et al demonstrated that miR‑592 acts as an oncogene and promotes Medullary thyroid carcinoma (MTC) tumorigenesis by decreasing the expression of cyclin‑dependent kinase 8 (CDK8) [ 11 ]. In 2021, Wang et al showed that a novel identified long non-coding RNA MEF2C-AS1 can inhibit Cervical Cancer (CC) through suppressing miR-592 by targeting R-spondin1 (RSPO1) [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

“…In 2018, He et al shown that miR-592 can promote the proliferation, migration, and invasion of gastric cancer through the PI3K/AKT and MAPK/ERK signaling pathways by targeting Spry2 [ 10 ]. In 2020, Liu et al demonstrated that miR‑592 acting as an oncogene can promote medullary thyroid cancer tumorigenesis by targeting cyclin‑dependent kinase 8 [ 11 ]. Recent study has shown that compared with those with lowgrade UVM patients, miR‑592 expression in UVM patients with highgrade was significantly increased [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-592 serves as a novel tumor suppressor in Uveal melanoma: bioinformatics analysis and in vitro cell function verification

Lei

Xue

et al. 2022

Bioengineered

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Uveal melanoma (UVM), one common eye tumor in adults, is related with a high risk of metastasis and poor prognosis. Studies have shown that many miRNAs are abnormally expressed in UVM tissues, and play an important regulatory role in the cell proliferation, invasion, and metastasis of UVM. Therefore, it is of great significance to analyze the expression characteristics of microRNAs (miRNAs) in UVM and clarify the role of miRNA in the tumorigenesis and development of UVM. In this study, we firstly downloaded and analyzed miRNA expression data of UVM tissues in TCGA (The Cancer Genome Atlas) database to select the differential expressed miRNAs in different clinical stages (IIA, IIB, IIIA, IIIB, IV). Compared with other stages, microRNA-592 (miR-592) was up-regulated in stage IV UVM patients. Then we used several bioinformatics tools including miRbase, miRDB, RNA22 and TargetScan, and found that it was be conserved in different species. Cell viability was determined by Cell Counting Kit-8. The proliferation and invasion of MUM-2B and C819 cells was measured using Edu assay and Transwell assay. We found that silencing miR-592 enhanced the progression of UVM cells, while miR592 overexpression inhibited the cell growth and invasion. The target genes of miR-592 were predicted by three webservers (miRDB, RNA22, and TargetScan), and verified by Real-Time PCR (qPCR). This is the first study to explore the role of miR-592 in malignant progression of UVM by bioinformatics and cell experiments. Our study suggests that tumor suppressor miR-592 may function as potential therapeutic target and biomarker for UVM.

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“…In the previous study, miR-592 has been identified as a tumor suppressor or an oncogene in different types of cancer [Fu et al, 2016;Hou et al, 2017;He et al, 2018;Liu et al, 2020]. With regard to regulation of cell differentiation, gain-and loss-of-function approaches have demonstrated that miR-592 could induce astrocyte differentiation arrest in rat neural progenitor cells and predisposes them toward neurogenesis [Zhang et al, 2013].…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of miR-7a-5p and miR-592 during Expansion of Rat Dental Pulp Stem Cells and Their Implication in Osteogenic Differentiation

Rong

Rome

Yao³

2021

Cells Tissues Organs

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Dental pulp stem cells (DPSCs) possess strong osteogenic differentiation potential and are promising cell sources in regenerative medicine. However, such differentiation capacity progressively declines during their in vitro expansion. MicroRNAs (miRNAs) play important roles in modulating stem cell differentiation. This study aimed (1) to determine if miR-7a-5p and miR-592 are involved in maintaining and regulating osteogenic differentiation of DPSCs, and (2) to explore their potential regulatory pathways. We found that the expression of miR-7a-5p and miR-592 was significantly upregulated during the expansion of rat DPSCs (rDPSCs). Overexpression of these miRNAs inhibited the osteogenic/odontogenic differentiation of rDPSCs, as evidenced by calcium deposition and osteogenic/odontogenic gene expression. RT-qPCR determined that miR-592 could downregulate heat shock protein B8, whose expression is reduced during the expansion of rDPSCs. Furthermore, RNA-seq and bioinformatics analysis identified significant signaling pathways of miR-7a-5p and miR-592 in regulating osteogenic differentiation, including TNF, MAPK, and PI3K-Akt pathways. We conclude that upregulating miR-7a-5p and miR-592 suppresses the osteogenic differentiation of rDPSCs during their in vitro expansion, likely via TNF, MAPK, and PI3K-Akt pathways. The results may shed light on application of miR-7a-5p and miR-592 for maintaining osteo-differentiation potential in stem cells for bone regeneration and bone-related disease treatment.

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miR‑592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin‑dependent kinase 8

Cited by 6 publications

References 53 publications

Identification of m7G Methylation-Related miRNA Signature Associated with Survival and Immune Microenvironment Regulation in Uterine Corpus Endometrial Carcinoma

Identification of m7G Methylation-Related miRNA Signature Associated with Survival and Immune Microenvironment Regulation in Uterine Corpus Endometrial Carcinoma

MicroRNA-592 serves as a novel tumor suppressor in Uveal melanoma: bioinformatics analysis and in vitro cell function verification

Increased Expression of miR-7a-5p and miR-592 during Expansion of Rat Dental Pulp Stem Cells and Their Implication in Osteogenic Differentiation

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