MiR-592 suppresses the development of glioma by regulating Rho-associated protein kinase

Gao, Shanshan; Chen, Jian; Wang, Yuxia; Zhong, Yanhua; Dai, Qingfu; Wang, Qi; Tu, Jiancheng

doi:10.1097/wnr.0000000000001124

Cited by 20 publications

(17 citation statements)

References 24 publications

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“…22 Additionally, ROCK1 was also found to be involved in the regulation of glioma development. 23,24 Thus, we further explored whether miR-206 or ROCK1 were implicated in propofol-mediated regulation on glioma cells.…”

Section: Introductionmentioning

confidence: 99%

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Wang¹,

Yang²,

Liu³

et al. 2020

OTT

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Background: Propofol has been identified to perform anti-tumor functions in glioma. However, the molecular mechanisms underlying propofol-induced prevention on migration and invasion of glioma cells remain unclear. Methods: Cell proliferation, invasion and migration were measured by 3-(4,5)-dimethylthiahiazo (−z-y1)-3,5-di-phenytetrazoliumromide assay and transwell assay, respectively. The expression of microRNA (miR)-206 and Rho-associated coiled coil-containing protein kinase 1 (ROCK1) was detected by quantitative real-time polymerase chain reaction. Western blot was used to measure the activation of the PI3K/AKT pathway. The interaction between miR-206 and ROCK1 was analyzed using the dual-luciferase reporter assay, RNA immunoprecipitation assay, and pull-down assay. Results: Propofol treatment inhibited the migration, invasion, and PI3K/AKT pathway activation in glioma cells. MiR-206 was decreased in glioma tissues and cells, while propofol exposure induced the upregulation of miR-206 in glioma cells. Besides that, we also found overexpressed miR-206 enhanced propofol-mediated inhibition on the migration, invasion, and PI3K/AKT pathway activation of glioma cells. Subsequently, ROCK1 was confirmed to be a target of miR-206. ROCK1 was elevated in glioma tissues and cells, but was reduced by propofol exposure in glioma cells. The rescue assay indicated that the miR-206/ROCK1 axis was involved in propofol-induced inhibition on the migration, invasion, and PI3K/AKT pathway activation in glioma cells. Conclusion: Propofol inhibited the migration and invasion of glioma cells by blocking the PI3K/AKT pathway through the miR-206/ROCK1 axis, suggesting an effective clinical implication for the anesthetic to prevent the metastasis of glioma.

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Section: Introductionmentioning

confidence: 99%

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Wang¹,

Yang²,

Liu³

et al. 2020

OTT

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“…The biological impact of miR-592 has been reported across several malignancies, including breast, gastric and non-small cell lung cancer ( 26 – 28 ); however, whether miR-592 takes on the role of an oncogene or tumor suppressor is dependent on the tumor context. For example, miR-592 has been reported to be significantly downregulated in glioma, suppressing the development of glioma by regulating Rho-associated protein kinase ( 29 ). However, He et al ( 27 ) demonstrated that miR-592 is upregulated in gastric cancer (GC), promoting GC cell proliferation, migration and invasion, while inducing endothelial-to-mesenchymal transition via the phosphoinositide 3-kinase/AKT and mitogen-activated protein kinase/extracellular signal-regulated kinase signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Serum microRNA‑592 serves as a novel potential biomarker for early diagnosis of colorectal cancer

Pan

2020

Oncol Lett

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Colorectal cancer (CRC) is the second leading cause of cancer-associated mortality worldwide. Currently, available diagnostic biomarkers are neither sensitive nor specific. Thus, the present study aimed to identify novel circulating microRNAs (miRNAs) as biomarkers for the early diagnosis of CRC. All samples were provided by The Second Affiliated Hospital of Nanjing Medical University (Nanjing, China). Analysis of the GSE108153 and GSE55139 datasets, downloaded from the Gene Expression Omnibus (GEO) database was performed using the online tool, GEO2R. Reverse transcription-quantitative PCR was performed to determine miR-592 expression in CRC tissues, cells and serums of patients. Subsequently, the diagnostic value of serum miR-592 was assessed via receiver operating characteristic (ROC) curve analysis. Both the assessment of clinical samples and bioinformatics analysis demonstrated that miR-592 expression levels were significantly upregulated in the tissues and serum of patients with CRC, suggesting that elevated serum miR-592 may be tumor-derived. ROC analysis indicated that serum miR-592 levels may differentiate patients with early stage CRC and advanced adenoma from healthy individuals, with area under the curve values of 0.801 and 0.747, respectively. Taken together, the results of the present study suggest that serum miR-592 may be implicated as a potential biomarker for the early diagnosis of CRC.

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“…The expression of miR-592 is decreased in breast cancer and is associated with malignant clinicopathological characteristics (24). miR-592 expression was also reported to be reduced in glioma (25,26) and hepatocellular carcinoma (27)(28)(29). On the contrary, miR-592 is upregulated in prostate (30) and colorectal (31,32) cancers.…”

Section: Discussionmentioning

confidence: 99%

“…miR-592 exerts an inhibitory role in breast cancer through regulating cell growth and metastasis in vitro, as well as tumor growth in vivo (24). miR-592 was also identified as a tumor-suppressing miRNA in non-small cell lung cancer (23), glioma (25,26), and hepatocellular carcinoma (27)(28)(29), serving dispensable roles in regulating a wide range of biological behaviors. On the contrary, miR-592 was found to play tumor-promoting roles in prostate (30) and colorectal (31,32) cancers.…”

Section: Discussionmentioning

confidence: 99%

“…downregulation of miR-592 has frequently been observed in multiple human cancer types, including non-small cell lung cancer (23), breast cancer (24), glioma (25,26), hepatocellular carcinoma (27)(28)(29), prostate cancer (30), and colorectal cancer (31,32). However, its expression profile and functions in thyroid cancer are yet to be determined.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-592 suppresses the malignant phenotypes of thyroid cancer by regulating lncRNA NEAT1 and downregulating NOVA1

et al. 2019

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Numerous studies have demonstrated that various microRNAs (miRs) are aberrantly expressed in thyroid cancer and play critical roles in thyroid cancer malignancy. The aberrant expression of miR-592 has frequently been reported in multiple human cancer types; however, its expression profile and functions in thyroid cancer remain poorly understood. Reverse transcription-quantitative polymerase chain reaction was carried out to determine the expression profile of miR-592 in thyroid cancer tissues and cell lines. The regulatory effects of miR-592 upregulation on thyroid cancer cell proliferation, migration, and invasion in vitro, and tumor growth in vivo were investigated using a ccK-8 assay, migration and invasion assays, and a xenograft tumor model, respectively. Furthermore, the mechanisms underlying miR-592-mediated suppression of the aggressive phenotypes of thyroid cancer cells were explored in detail. The results indicated that miR-592 was significantly downregulated in thyroid cancer samples, and its downregulation was associated with lymph node metastasis and tumor-node-metastasis stage. Patients with thyroid cancer and low miR-592 expression exhibited shorter overall survival than patients with high miR-592 expression. Overexpression of miR-592 resulted in decreased cell proliferation, migration, and invasion in thyroid cancer. In addition, neuro-oncological ventral antigen 1 (NOVA1) was identified as a novel target gene of miR-592 in thyroid cancer cells. Furthermore, ectopic NOVA1 expression may effectively abolish the tumor-suppressing effects of miR-592 overexpression in thyroid cancer cells. Notably, the lncRNA NEAT1 was proposed to function as a sponge of miR-592 in thyroid cancer cells, thereby regulating NOVA1 expression. Finally, resuming miR-592 expression significantly impaired thyroid cancer tumor growth in vivo. The results indicated that the NEAT1/miR-592/NOVA1 pathway may play regulatory roles in thyroid cancer malignancy in vitro and in vivo. Our findings may provide novel insight into the pathogenesis of thyroid cancer. Therefore, this pathway may be an effective target for treating patients with this disease.

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MiR-592 suppresses the development of glioma by regulating Rho-associated protein kinase

Cited by 20 publications

References 24 publications

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Serum microRNA‑592 serves as a novel potential biomarker for early diagnosis of colorectal cancer

MicroRNA-592 suppresses the malignant phenotypes of thyroid cancer by regulating lncRNA NEAT1 and downregulating NOVA1

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