Tumour suppressor microRNA-584 directly targets oncogene Rock-1 and decreases invasion ability in human clear cell renal cell carcinoma

Ueno, Koji; Hirata, Hiroshi; Shahryari, Varahram; Chen, Y; Zaman, Mohd Saif; Singh, Kamaldeep; Tabatabai, Z. Laura; Hinoda, Yuji; Dahiya, Rajvir

doi:10.1038/sj.bjc.6606028

Cited by 93 publications

(73 citation statements)

References 30 publications

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“…Xiang et al reported that ectopic expression of miR-584 attenuated neuroblastoma cell groWTh, migration, invasion, and angiogenesis in vitro (38). Ueno et al revealed that miR-584 overexpression decreased cell motility in clear cell renal cell carcinoma (21). Moreover, Orlandella et al showed that resumed expression of miR-584 inhibited the migration and invasion of thyroid carcinoma cells and induced their resistance to apoptosis (22,23).…”

Section: Discussionmentioning

confidence: 99%

“…Multiple targets of miR-584 have been validated, including WWP1 (37) in gastric cancer, MMP14 (38) in neuroblastoma, ROCK1 (21) in clear cell renal cell carcinoma, TUSC2 (23) and ROCK1 (22) in thyroid carcinoma, and PTTG1IP (24) and ROCK1 (39,40) in glioma. These studies suggest that miR-584 exhibits tissue-specific functions.…”

Section: Discussionmentioning

confidence: 99%

“…MiR-584 functions as tumour suppressor in several types of cancer (21)(22)(23)(24). In NSCLC, miR-584 expression was reported to be downregulated in tissue samples (25) and upregulated in the plasma of NSCLC patients (26).…”

Section: Microrna-584 Inhibits Cell Proliferation and Invasion In Nonmentioning

confidence: 99%

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MicroRNA-584 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting MTDH

Zhang

Wang

2017

Exp Ther Med

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Abstract. Lung cancer is the third most frequent human malignant tumour and the leading cause of cancer-associated mortality worldwide. Emerging lines of evidence have demonstrated that microRNAs (miRNAs) are upregulated or downregulated in non-small cell lung cancer (NSCLC), and this phenomenon is involved in the regulation of various processes during tumorigenesis and progression, including tumour groWTh, apoptosis, cell invasion, and tumour metastasis. Therefore, understanding the molecular mechanism that associates abnormally expressed miRNAs with NSCLC formation and development may lead to the identification of novel diagnostic, and therapeutic targets for patients with NSCLC. miRNA-584 (miR-584) functions as a tumour suppressor in several types of cancer. However, the expression pattern, detailed biological function and underlying molecular mechanism of miR-584 in NSCLC remain unclear. Therefore, the present study detected the expression of miR-584 in NSCLC, investigated its role in NSCLC cells and determined its underlying molecular mechanism. In the current study, it was demonstrated that miR-584 was downregulated in NSCLC tissues and cell lines. Low miR-584 expression was correlated with tumour size, tumour node metastasis stage and distant metastasis. Overexpression of miR-584 inhibited cell proliferation and invasion in NSCLC. Additionally, metadherin was identified as a direct target gene of miR-584 in NSCLC as confirmed by a series of experiments. Moreover, upregulation of miR-584 was involved in the regulation of the phosphatase and tensin homolog/Akt serine/threonine kinase signalling pathway in NSCLC. Thus, miR-584 may serve as a tumor-suppressor, and the results of the present study provide a reference for future research into the potential mechanisms underlying NSCLC progression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MicroRNA-584 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting MTDH

Zhang

Wang

2017

Exp Ther Med

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“…Together with this, in this study, we found that miR-148a could target this signaling pathway through downregulating ROCK1, and high ROCK1 expression was associated with low miR-148a levels in gastric cancer, bringing a new insight about the essential mechanisms of regulating the Rho-ROCK pathway in gastric cancer. In addition, miR-146a and miR-584 are also proved to target ROCK1 in prostate cancer and clear cell renal cell carcinoma, respectively (34,35). miR-139 and miR-124 Figure 5.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-148a Suppresses Tumor Cell Invasion and Metastasis by Downregulating ROCK1 in Gastric Cancer

Zheng

Liang

Wang

et al. 2011

Clinical Cancer Research

249

207

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Purpose: MicroRNAs (miRNA) have been documented playing a critical role in cancer development and progression. In this study, we investigate the role of miR-148a in gastric cancer metastasis.Experimental Design: We examined miR-148a levels in 90 gastric cancer samples by qRT-PCR and analyzed the clinicopathologic significance of miR-148a expression. The gastric cancer cells stably expressing miRNA-148a were analyzed for migration and invasion assays in vitro and metastasis assays in vivo; the target genes of miR-148a were further explored.Results: We found that miR-148a expression was suppressed by more than 4-fold in gastric cancer compared with their corresponding nontumorous tissues, and the downregulated miR-148a was significantly associated with tumor-node-metastasis (TNM) stage and lymph node-metastasis. Functional assays showed that overexpression of miR-148a suppressed gastric cancer cell migration and invasion in vitro and lung metastasis formation in vivo. In addition, overexpression of miR-148a in GC cells could reduce the mRNA and protein levels of ROCK1, whereas miR-148a silencing significantly increased ROCK1 expression. Luciferase assays confirmed that miR-148a could directly bind to the 2 sites of 3 0 untranslated region of ROCK1. Moreover, in gastric cancer tissues, we observed an inverse correlation between miR-148a and ROCK1 expression. Knockdown of ROCK1 significantly inhibited gastric cancer cell migration and invasion resembling that of miR-148a overexpression. We further found that ROCK1 was involved in miR-148a-induced suppression of gastric cancer cell migration and invasion. Conclusions: miR-148a functions as a tumor metastasis suppressor in gastric cancer, and downregulation of miR-148a contributes to gastric cancer lymph node-metastasis and progression. miR-148a may have a therapeutic potential to suppress gastric cancer metastasis. Clin Cancer Res; 17(24); 7574-83. Ó2011 AACR.

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“…In this study, we identified miR-584, a potential tumor suppressor (32), as a novel target of TGF-␤ and found that miR-584 expression was negatively regulated by this growth factor in a number of breast cancer cells. We found the inhibition of miR-584 expression by TGF-␤ to be required for cell migration as overexpression of ectopic miR-584 could reverse TGF-␤-induced cell migration.…”

mentioning

confidence: 99%

MicroRNA-584 and the Protein Phosphatase and Actin Regulator 1 (PHACTR1), a New Signaling Route through Which Transforming Growth Factor-β Mediates the Migration and Actin Dynamics of Breast Cancer Cells

Fils-Aimé

Dai

Guo

et al. 2013

Journal of Biological Chemistry

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Background: TGF-␤ promotes cell migration in advanced breast cancer. Results: TGF-␤ down-regulates miR-584, leading to a PHACTR1 overexpression, and both are involved in cell migration and actin reorganization. Conclusion:The regulation of miR-584 and regulation of its novel target PHACTR1 are necessary steps for breast cancer cell migration. Significance: MicroRNAs offer an interesting therapeutic target in the treatment of advanced breast malignancy.

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Tumour suppressor microRNA-584 directly targets oncogene Rock-1 and decreases invasion ability in human clear cell renal cell carcinoma

Cited by 93 publications

References 30 publications

MicroRNA-584 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting MTDH

MicroRNA-584 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting MTDH

MicroRNA-148a Suppresses Tumor Cell Invasion and Metastasis by Downregulating ROCK1 in Gastric Cancer

MicroRNA-584 and the Protein Phosphatase and Actin Regulator 1 (PHACTR1), a New Signaling Route through Which Transforming Growth Factor-β Mediates the Migration and Actin Dynamics of Breast Cancer Cells

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