MicroRNA-153 suppresses cell invasion by targeting SNAI1 and predicts patient prognosis in glioma

Zhao, Wei; Yin, Changyou; Jiang, Jing; Kong, Wei; Xu, Hao; Zhang, Hongtao

doi:10.3892/ol.2018.9706

Cited by 10 publications

(10 citation statements)

References 26 publications

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“…miR-153, as one of the conservative miRNAs, was initially found in seven miRNAs specifically expressed in human and mouse brain tissues. 26 Current studies have confirmed that miR-153 is involved in the development and progression of a variety of malignancies, [27][28][29][30][31][32] such as prostate carcinoma, colorectal cancer, hepatocellular malignancy, non-small-cell lung carcinoma, gastric malignant tumor, glioma and BC. However, its role in various tumors is not exactly identical.…”

Section: Discussionmentioning

confidence: 94%

“…31 miR-153 inhibits glioma progression by directly regulating SNAI1 and downregulation of miR-153 is related to poor prognosis in glioma sufferers. 32 Therefore, these evidence suggest that the biological behavior of miR-153 seems to have cell and tissue specificity, playing distinct roles in different tumors. With regard to the study of miR-153 in BC, Li et al have reported that miR-153 suppresses EMT of BC via targeting MTDH.…”

Section: Discussionmentioning

confidence: 97%

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<p>Upregulation Of miR-153 Inhibits Triple-Negative Breast Cancer Progression By Targeting ZEB2-Mediated EMT And Contributes To Better Prognosis</p>

Shi

Fan

et al. 2019

OTT

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Background: Triple-negative breast cancer (TNBC) is the most malignant type of breast cancer. MicroRNAs (miRs) and their corresponding molecular targets are associated with the occurrence and development of various human malignancies. However, the roles of the microRNA-153 (miR-153) and zinc finger E-box-binding homeobox 2 (ZEB2)-induced epithelial-mesenchymal transition (EMT) in TNBC and predictive effect of miR-153 on the prognosis of TNBC have not been fully elucidated. Materials and methods: Relative miR-153 expression level was examined by RT-qPCR assay in TNBC tissues of 60 patients and TNBC cell lines (SKBR3, BT-549 and MDA-MB-231). Cell proliferation ability, invasion ability and migration ability were measured by CCK8 assay, Transwell invasion assay and wound healing assay, respectively. Luciferase reporting experiment was used to confirm that there was a miR-153-binding site in ZEB2 3ʹ-UTR. The expression of ZEB2 in tissues and its relationship with miR-153 were analyzed with immunohistochemistry method. Relative ZEB2, E-cadherin, N-cadherin and Vimentin mRNA and protein expression levels were observed with RT-qPCR and Western blot, respectively. Based on risk factors, a prognostic model was established according to the Cox proportional risk model, and the prognostic risk factors of TNBC patients were predicted and analyzed. Results: The expression of miR-153 in TNBC tissues and cells was declined (all P<0.01), and upregulation of miR-153 inhibited proliferation, invasion and migration of TNBC cells (all P<0.01). In addition, miR-153 regulated ZEB2/EMT link in TNBC, and ZEB2 overexpression reversed the tumor-suppressive effect of miR-153 in TNBC. Moreover, miR-153 was an independent predictive factor that was associated with excellent prognosis in TNBC patients. Conclusion: miR-153 may inhibit TNBC proliferation, invasion and migration by regulating ZEB2/EMT link. Therefore, miR-153 is expected to be a molecular target and prognostic marker for TNBC.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 97%

<p>Upregulation Of miR-153 Inhibits Triple-Negative Breast Cancer Progression By Targeting ZEB2-Mediated EMT And Contributes To Better Prognosis</p>

Shi

Fan

et al. 2019

OTT

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“…However, in some other cancer types, the expression of miR-153 is decreased, playing a role of tumor suppressor. For example, Zhao et al [12] found that miR-153 was down-regulated in glioma tissues and cells versus paracancerous tissues and normal immortalized gliocyte HEB cells. They verified that SNAI1 was a target of miR-153 and had a negative association with miR-153 detected by luciferase reporter assay.…”

Section: Discussionmentioning

confidence: 99%

“…Deregulation of miR-153 has recently been observed in several common human cancer, while miR-153 serves an oncogene [10,11] or tumor suppressive [12–17] role in different cancer types. Previously, miR-153 has been identified to be overexpressed in prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

Increased expression of miR-153 predicts poor prognosis for patients with prostate cancer

Zhang

Bai

et al. 2019

Medicine

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Deregulation of miR-153 has recently been observed in several common human cancer, while miR-153 serves an oncogene or tumor suppressive role in different cancer types. Previously, miR-153 has been identified to be overexpressed in prostate cancer. miR-153 played an important role in promoting proliferation of human prostate cancer cells and presented a novel mechanism of microRNA-mediated direct suppression of phosphatase and tensin homolog (PTEN) expression in prostate cancer cells. Until now, little is known about the clinical significance of miR-153 expression in prostate cancer.The miR-153 expression in 143 pairs of prostate cancer and adjacent non-cancerous prostate tissues was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis. Student t test was conducted for intergroup comparison. Pearson correlation test was used for correlation analysis. Survival curves were carried out by the Kaplan–Meier method and evaluated using the log-rank test. Multivariable Cox proportional hazard risk regression model was performed to screen the independent factor affected the prognosis of prostate cancer patients.qRT-PCR analysis showed that the expression of miR-153 was significantly increased in the prostate cancer tissues in comparison with the adjacent noncancerous prostate tissues (P < .001). The high expression of miR-153 in prostate cancer tissues is closely correlated with aggressive clinical pathological parameters such as lymph node metastasis (P = .001); bone metastasis (P < .001); Gleason score (P < .001); and tumor-node-metastasis (TNM) stage (P < .001). Prostate cancer patients with a high expression of miR-153 had an evidently lower 5-year overall survival as compared with those with a low expression of miR-153 (P = .019). Notably, the multivariate Cox regression analysis indicated that miR-153 expression was an independent factor for predicting the 5-year overall survival of prostate cancer patients (hazard ratio [HR] = 2.481, 95% confidence interval [CI]: 1.582–10.727; P = .018).Our study demonstrated that high miR-153 expression was significantly associated with a poor overall survival independently of other factors in prostate cancer. Therefore, miR-153 may be an available biomarker for prostate cancer prognosis.

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“…Glioma is the most common form of brain cancer (1), and the prognosis of glioma is relatively poor (2). Glioma cells infiltrate the healthy tissues surrounding the main tumor mass, limiting the survival of patients with glioma (3).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑769‑3p inhibits tumor progression in glioma by suppressing ZEB2 and inhibiting the Wnt/β‑catenin signaling pathway

Wang¹,

Yang

Gao³

et al. 2019

Oncol Lett

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Accumulating evidence suggests the crucial role of microRNAs (miRNAs) in human cancers. The present study aimed to investigate the clinical and functional roles of miR-769-3p in glioma, as well as the underlying molecular mechanisms. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine the expression levels of miR-769-3p in glioma tissues and cells. Receiver operating characteristic (ROC) curve analysis was applied to calculate the diagnostic value of miR-769-3p. The 5-year survival rate of patients was calculated using Kaplan-Meier analysis and Cox regression analysis. Cell experiments were used to investigate the functional role of miR-769-3p in glioma. The gene target of miR-769-3p was predicted by TargetScan. Changes in the levels of Wnt signaling-related proteins were measured by western blotting. miR-769-3p was significantly downregulated in glioma tissues and serum, as well as in glioma cell lines (P<0.001). miR-769-3p expression was significantly associated with the World Health Organization grade and Karnofsky performance score. The ROC curves demonstrated that serum miR-769-3p level reliably distinguished patients with glioma from healthy individuals. High tissue miR-769-3p expression predicted poor overall survival in patients with glioma (log-rank P=0.001) and was identified as an independent prognostic factor. In addition, zinc finger E-box binding homeobox 2 (ZEB2) was demonstrated to be a direct target of miR-769-3p in glioma cells using a luciferase assay. miR-769-3p upregulation suppressed the activity of the Wnt/β-catenin signaling pathway in glioma cells. In conclusion, miR-769-3p may serve as a diagnostic and prognostic biomarker in patients with glioma and target ZEB2 to inhibit tumor progression via the Wnt/β-catenin signaling pathway. miR-769-3p may be a novel therapeutic target for the treatment of glioma.

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MicroRNA-153 suppresses cell invasion by targeting SNAI1 and predicts patient prognosis in glioma

Cited by 10 publications

References 26 publications

<p>Upregulation Of miR-153 Inhibits Triple-Negative Breast Cancer Progression By Targeting ZEB2-Mediated EMT And Contributes To Better Prognosis</p>

<p>Upregulation Of miR-153 Inhibits Triple-Negative Breast Cancer Progression By Targeting ZEB2-Mediated EMT And Contributes To Better Prognosis</p>

Increased expression of miR-153 predicts poor prognosis for patients with prostate cancer

MicroRNA‑769‑3p inhibits tumor progression in glioma by suppressing ZEB2 and inhibiting the Wnt/β‑catenin signaling pathway

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