MiRNA-20a-5p promotes the growth of triple-negative breast cancer cells through targeting RUNX3

Bai, Xuejuan; Han, Guohui; Liu, Yang; Jiang, Hongchuan; He, Qiang

doi:10.1016/j.biopha.2018.04.165

Cited by 83 publications

(68 citation statements)

References 28 publications

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“…miR-143 was found to be upregulated in mesenteric fat of high-fat diet-induced mice (18). miR-20a-5p, as a member of the miR-17-92 gene cluster, has critical roles in tumorigenesis and development (19,20). We have recently demonstrated that miR-20a-5p regulates adipogenesis in preadipocytes as well as marrow stromal cells (21,22).…”

Section: Introductionmentioning

confidence: 99%

A Novel Regulatory Circuit “C/EBPα/miR-20a-5p/TOB2” Regulates Adipogenesis and Lipogenesis

et al. 2020

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Recent studies have identified growing importance of microRNAs as key regulators of adipocyte differentiation. We have previously reported that miR-20a-5p is able to induce adipogenesis of established adipogenic cell lines and bone marrow derived mesenchymal stem cells (BMSCs). However, the molecular mechanisms by which miR-20a-5p controls adipogenesis and by which miR-20a-5p expression is regulated need to be further explored. In the current study we found that miR-20a-5p expression was induced during adipocyte differentiation from preadipocyte 3T3-L1 and was increased in epididymal white adipose tissue from either ob/ob mice or high fat diet-induced obese mice. Functional studies identified miR-20a-5p as a positive regulator of adipocyte differentiation and lipogenesis in 3T3-L1 by using either synthetic mimics to supplement miR-20a-5p, or using synthetic inhibitor or sponge lentivirus to inactivate endogenous miR-20a-5p. Luciferase activity assay revealed that TOB2 is a novel target of miR-20a-5p and functional experiment demonstrated its negative regulatory role in adipocyte differentiation. Moreover, Tob2 overexpression significantly attenuated adipocyte formation induced by miR-20a-5p supplementation. In-depth investigation of mechanisms that govern miR-20a-5p expression clarified that C/EBPα transcriptionally activated miR-20a-5p expression via binding to the promoter of miR-20a-5p. Taken together, we conclude that a novel C/EBPα/miR-20a-5p/TOB2 circuit exists and regulates adipogenesis and lipogenesis.

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Section: Introductionmentioning

confidence: 99%

A Novel Regulatory Circuit “C/EBPα/miR-20a-5p/TOB2” Regulates Adipogenesis and Lipogenesis

et al. 2020

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“…Indeed, cell viability and epithelial-mesenchymal transition-promoting properties of miR-221-3p were already described, together with its ability to induce cell proliferation of TNBC cells [73], a characteristic feature known also for another four highly expressed miRNAs: miR-181b-5p, miR-21-3p, miR-25-3p, and miR-27a-3p [44,47,74,75]. Moreover, highly expressed miRNAs miR-103-3p, miR-181b-5p, miR-20a-5p, miR-21a-3p, miR-221-3p, and miR-27a-3p are involved in regulation of TNBC cells migration [44][45][46][73][74][75], whereas miR-103-3p, miR-20a-5p, and miR-27a-3p have been previously associated with invasion of TNBC cells [45,46,75]. A high expression of another two miRNAs, miR-221-3p and miR-27a-3p, was previously correlated with poor TNBC patient survival [40,42].…”

Section: Discussionmentioning

confidence: 98%

“…A comparison of the top expressed tRNAs, snoRNAs, snRNAs, and piRNAs revealed similar result, with a share of the highly expressed molecules (46,13,14, and 9 tRNAs, snoRNAs, snRNAs, and piRNAs, respectively) common for all cell lines (Supplementary Figure S2). We further analyzed whether any of the highly expressed miRNAs were previously associated with TNBC and found that seven out of the 83 miRNAs, common for all three cell lines (miR-181b-5p, miR-221-3p, miR-27a-3p, miR-21-3p, miR-20a-5p, miR-103a-3p and miR-25-3p), have been previously associated with the TNBC phenotype [39][40][41][42][43][44][45][46][47] Another three molecules, miR-210-3p, miR-155-5p and miR-125b-5p, highly expressed in HCC1806 and Hs 578T cells, are known as hallmarks of TNBC [40,41,48,49], whereas miR-342-3p, highly expressed exclusively in basal-like TNBC cell lines, has been previously described as an important regulator of molecular mechanisms of this breast cancer subtype [50]. Interestingly, miRNAs miR-101-3p, miR-17-5p, miR-93-5p, miR-340-5p, and miR-31-5p, known mainly for their tumor suppressor properties, were found among the top expressed miRNAs in our dataset [51][52][53][54][55][56][57][58].…”

Section: Characterization Of Small Non-coding Rna Expression Profile mentioning

confidence: 99%

Small Non-Coding RNA Profiling Identifies miR-181a-5p as a Mediator of Estrogen Receptor Beta-Induced Inhibition of Cholesterol Biosynthesis in Triple-Negative Breast Cancer

Alexandrova

Lamberti

Saggese

et al. 2020

Cells

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Triple-negative breast cancer (TNBC) is a highly heterogeneous disease, representing the most aggressive breast cancer (BC) subtype with limited treatment options due to a lack of estrogen receptor alpha (ERα), progesterone receptor (PR), and Erb-B2 receptor tyrosine kinase 2 (HER2/neu) expression. Estrogen receptor beta (ERβ) is present in a fraction of TNBC patients, where its expression correlates with improved patient outcomes, supported by the fact that it exerts oncosuppressive effects in TNBC cell models in vitro. ERβ is involved in microRNA-mediated regulation of gene expression in hormone-responsive BC cells and could mediate its actions through small noncoding RNAs (sncRNAs) in TNBCs also. To verify this possibility, smallRNA sequencing was performed on three ERβ-expressing cell lines from different TNBC molecular subtypes. Several sncRNAs resulted modulated by ERβ, with a subset being regulated in a tumor subtype-independent manner. Interestingly, sncRNA profiling of 12 ERβ+and 32 ERβ− primary TNBC biopsies identified 7 microRNAs, 1 PIWI-interacting RNA (piRNA), and 1 transfer RNA (tRNA) differentially expressed in ERβ+ compared to ERβ− tumors and cell lines. Among them, miR-181a-5p was found to be overexpressed in ERβ+ tumors and predicted target key components of the cholesterol biosynthesis pathway previously found to be inhibited by ERβ in TNBC cells.

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“…The expression of miR-20a in glioma, cervical cancer, gastric cancer, lung carcinoma, neuroblastoma and prostate cancer, and its corresponding target genes and their functions, are presented in Table II (46,(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60)(61)(62)(63)(64)(65)(66)(67)(68). However, the upregulation or downregulation of miR-20a expression in a number of tumors is not consistent in numerous previous studies due to the differences in cell lines and limited sample sizes (47,(69)(70)(71)(72)(73)(74)(75)(76)(77)(78)(79). The current review article outlines the role of miR-20a in CRC and provides information that can be used in future research on miR-20a.…”

Section: Microrna-20a Overviewmentioning

confidence: 89%

Function and mechanisms of microRNA‑20a in colorectal cancer (Review)

et al. 2020

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Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-associated mortality worldwide. CRC currently has no specific biomarkers to promote its diagnosis and treatment and the underlying mechanisms regulating its pathogenesis have not yet been determined. MicroRNAs (miRs) are small, non-coding RNAs that exhibit regulatory functions and have been demonstrated to serve a crucial role in the post-transcriptional regulatory processes of gene expression that is associated with cell physiology and disease progression. Recently, abnormal miR-20a expression has been identified in a number of cancers types and this has become a novel focus within cancer research. High levels of miR-20a expression have been identified in CRC tissues, serum and plasma. In a recent study, miR-20a was indicated to be present in feces and to exhibit a high sensitivity to CRC. Therefore, miR-20a may be used as a marker for CRC and an indicator that can prevent the invasive examination of patients with this disease. Changes in the expression of miR-20a during chemotherapy can be used as a biomarker for monitoring resistance to treatment. In conclusion, miR-20a exhibits the potential for clinical application as a novel diagnostic biomarker and therapeutic target for use in patients with CRC. The present study focused on the role and mechanisms of miR-20a in CRC. Contents 1. Introduction 2. microRNA-20a overview 3. The mechanism of miR-20a in CRC 4. miR-20a can be used as a diagnostic marker in CRC 5. miR-20a may be used as a monitoring indicator during chemotherapy 6. Conclusion and prospects

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MiRNA-20a-5p promotes the growth of triple-negative breast cancer cells through targeting RUNX3

Cited by 83 publications

References 28 publications

A Novel Regulatory Circuit “C/EBPα/miR-20a-5p/TOB2” Regulates Adipogenesis and Lipogenesis

A Novel Regulatory Circuit “C/EBPα/miR-20a-5p/TOB2” Regulates Adipogenesis and Lipogenesis

Small Non-Coding RNA Profiling Identifies miR-181a-5p as a Mediator of Estrogen Receptor Beta-Induced Inhibition of Cholesterol Biosynthesis in Triple-Negative Breast Cancer

Function and mechanisms of microRNA‑20a in colorectal cancer (Review)

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