MicroRNA-124 inhibits cellular proliferation and invasion by targeting Ets-1 in breast cancer

Li, Wentao; Zang, Wenqiao; Liu, Pei; Wang, Yuanyuan; Du, Yuwen; Chen, Xiaonan; Deng, Meng; Sun, Wencong; Wang, Lei; Zhao, Guoqiang; Zhai, Baoping

doi:10.1007/s13277-014-2402-2

Cited by 45 publications

(31 citation statements)

References 35 publications

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“…It has also been reported to function as an important regulator of many human cancers (43,44). In particular, recent studies have indicated that miR-124 targets specific genes to regulate proliferation and migration in breast cancer (45)(46)(47).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer

Sun

et al. 2016

Oncology Reports

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Abstract. MicroRNA (miRNA) is a type of endogenous non-coding RNA implicated in various cellular processes. Studies have shown that miR-124 is involved in the malignant progression of cancer, but little is known concerning its potential role in breast cancer. Therefore, the purpose of this study was to conduct a functional analysis of miR-124 in breast cancer, and to identify its target genes in this disease. To this end, we used quantitative real-time PCR to examine the expression level of miR-124 in breast cancer tissue specimens and cell lines. To study the functional significance of miR-124, we overexpressed miR-124 with miR-124 mimics and observed breast cancer cell proliferation, colony formation, migration, and invasion abilities by in vitro cell culture experiments. Target prediction algorithms and luciferase reporter gene assays were used to identify the target genes of miR-124. We also knocked down miR-124 targets using short hairpin RNA (shRNA) constructs, and observed associated breast cancer cell characteristics by in vitro cell culture experiments. We found that miR-124 expression significantly decreased in breast cancer tissues and cells compared to normal tissues and cells. In addition, cell proliferation, colony formation, migration, and invasion were decreased after overexpression of miR-124 in breast cancer cells. Furthermore, we used several algorithms to identify the snail family zinc finger 2 (SNAI2) as a potential target gene of miR-124. The protein expression level and luciferase activity of the 3'-untranslated region of SNAI2 were significantly decreased in breast cancer cells transfected with miR-124 mimics. Cell proliferation, colony formation, migration, and invasion were also decreased after knockdown of SNAI2 by shRNA. In conclusion, our data suggest that miR-124 expression is decreased in breast cancer and plays an important role as a tumor suppressor gene by targeting SNAI2. These findings may reveal novel perspectives for clinical treatments against breast cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer

Sun

et al. 2016

Oncology Reports

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“…miRNAs are short (approximately 22 bases) noncoding RNA molecules that post-transcriptionally regulate gene expression through incomplete base pairing with the 3′ UTR of target mRNAs [15]. They have been estimated to regulate up to 30% of all human genes and to control a variety of cellular processes [48]. In IgAN, there are few reports about the regulation of miRNAs in mesangial cells.…”

Section: Discussionmentioning

confidence: 99%

Proliferation and Cytokine Production of Human Mesangial Cells Stimulated by Secretory IgA Isolated from Patients with IgA Nephropathy

Liang

Zhou

Xing

et al. 2015

Cell Physiol Biochem

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Background/Aims: IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis, and often aggravates by mucosal infection. Secretory IgA (SIgA) is the dominant immunoglobulin in mucosal immunity, and is deposited in the mesangium in IgAN. The biological effects of SIgA on mesangial cells are poorly understood. Methods: Deposition of SIgA in frozen renal sections from IgAN patients was detected and the association between deposition of SIgA and patients characteristics was analyzed. The biological effects of SIgA and polymeric IgA (pIgA) on human renal mesangial cells were compared. We also studied the molecular mechanism of microRNA regulating the inflammatory effects of SIgA on mesangial cells. Results: Fifty-five of 176 patients had SIgA deposition with higher incidence of infection history and hematuria, lower serum cystatin C, β2 microglobulin, blood urea nitrogen and T-grade in the Oxford classification, compared with patients without SIgA deposition. SIgA stimulated mesangial cells at a higher ratio of proliferation and higher production of interleukin (IL)-6, IL-8, monocyte chemotactic protein 1, transforming growth factor-β1 and fibronectin, compared with SIgA from healthy volunteers. The proliferation and cytokines production in mesangial cells stimulated by SIgA were significantly lower than that stimulated by pIgA. miR-16 targeted the 3′-untranslated region of IL-6 and suppressed its translation in mesangial cells induced by SIgA. Conclusions: The biological effects of SIgA on mesangial cells differ from those of pIgA. SIgA stimulates mesangial cell proliferation and production of proinflammatory cytokines. IL-6 production is regulated by miR-16 in mesangial cells.

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“…They act as negative regulators of gene expression and play a crucial role in regulating breast cancer cell proliferation, invasion, migration and metastasis [5][6][7]. Accumulating data showed a number of miRNAs, such as miR-23 [8], miR-200 [9], miR-378 [10] were reported as key regulators in breast cancer.…”

Section: Introductionmentioning

confidence: 99%

MiR-132 prohibits proliferation, invasion, migration, and metastasis in breast cancer by targeting HN1

Zhang

Chen

et al. 2014

Biochemical and Biophysical Research Communications

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MicroRNA-124 inhibits cellular proliferation and invasion by targeting Ets-1 in breast cancer

Cited by 45 publications

References 35 publications

MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer

MicroRNA-124 inhibits cell proliferation and migration by regulating SNAI2 in breast cancer

Proliferation and Cytokine Production of Human Mesangial Cells Stimulated by Secretory IgA Isolated from Patients with IgA Nephropathy

MiR-132 prohibits proliferation, invasion, migration, and metastasis in breast cancer by targeting HN1

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