miR-3178 inhibits cell proliferation and metastasis by targeting Notch1 in triple-negative breast cancer

Kong, Pengfei; Chen, Lie; Yu, Mengxue; Ji, Tao; Liu, Jiawei; Wang, Yue; Pan, Hong; Zhou, Wenbin; Wang, Shui

doi:10.1038/s41419-018-1091-y

Cited by 48 publications

(40 citation statements)

References 51 publications

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“…However, emerging studies have confirmed that different miRNAs play diverse roles in TNBC, some as tumorigenic agents, and some as tumor inhibitors. For example, as tumorigenic agents, miR-25, 16 miR-20, 17 miR-224, 18 miR-135 19 and miR-301 20 promote the occurrence and development of TNBC, whereas miR-124, 15 miR-4417, 21 miR-4306, 22 miR-199, 23 miR-1287 24 and miR-3178 25 as tumor inhibitors inhibit the oncogenesis and development of TNBC. In this study, relative miR-153 expression in TNBC tissues and cells was remarkably lower than that in corresponding adjacent noncancerous tissues and normal breast epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

<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: 99%

<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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“…MiR-8084, miR-708-3p, miR-96-182-183 cluster, miR-484, miR-210, and miR-142-3p modulate the invasive potential of BC cells by modulating EMT [16][17][18][19]. Recently, it has been shown that miR-124, miR-199a/214, miR-3178, miR-30a, miR-508-3p and miR-212-5p can modulate the level of EMT markers and TFs regulating the expression of E-cadherin in TNBC, a subtype that commonly metastasizes to the brain [51][52][53]85].…”

Section: Mirna-mediated Activation Of Emtmentioning

confidence: 99%

“…Angiogenic factors and growth factors either released by tumor cells or stromal cells individually or during their mutual crosstalk contribute to intravasation [89]. These factors allow tumor cells to invade through the basement membrane, adhere to the endothelial membrane, and pass through endothelial gap junctions to Table 1 miRNAs mediated regulation of BCBM miRNA Targets Regulation References EMT miR-8084 ING2, p53-BAX upregulated [16] miR-484 PAX-5 upregulated [19] miR-708-3p ZEB1, CDH2 and vimentin downregulated [17] miR-210 E-cadherin (ORF), PAX-5 upregulated [19] miR-142-3p Bach-1, CXCR4, MMP9, and VEGFR downregulated [18] miR-199a/214 Slug downregulated [51] miR-3178 Notch1 downregulated [52] miR-212-5p Prrx2 downregulated [53] miR-143 PUMA upregulated [35] miR-125a-5p ICAM-1 downregulated [38] miR-1258 HPSE downregulated [40] miR-210 Occludin, β-catenin upregulated [37] Cross Talk and Niche Formation miR-26a PTEN ATM upregulated [70,71] miR-19a PTEN upregulated [42] disseminate into the circulation [86]. Although no miRNA has been reported to influence intravasation directly, they can regulate angiogenic signals by targeting angiogenic factors and protein kinases.…”

Section: Mirna-mediated Intravasationmentioning

confidence: 99%

microRNAs Orchestrate Pathophysiology of Breast Cancer Brain Metastasis: Advances in Therapy

et al. 2020

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Brain metastasis (BM) predominantly occurs in triple-negative (TN) and epidermal growth factor 2 (HER2)-positive breast cancer (BC) patients, and currently, there is an unmet need for the treatment of these patients. BM is a complex process that is regulated by the formation of a metastatic niche. A better understanding of the brain metastatic processes and the crosstalk between cancer cells and brain microenvironment is essential for designing a novel therapeutic approach. In this context, the aberrant expression of miRNA has been shown to be associated with BM. These non-coding RNAs/miRNAs regulate metastasis through modulating the formation of a metastatic niche and metabolic reprogramming via regulation of their target genes. However, the role of miRNA in breast cancer brain metastasis (BCBM) is poorly explored. Thus, identification and understanding of miRNAs in the pathobiology of BCBM may identify a novel candidate miRNA for the early diagnosis and prevention of this devastating process. In this review, we focus on understanding the role of candidate miRNAs in the regulation of BC brain metastatic processes as well as designing novel miRNA-based therapeutic strategies for BCBM.Keywords: Breast cancer brain metastasis, miRNA, Brain tumor microenvironment, Blood-brain barrier, CNS metastasis

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“…More targets regulated by miRNAs in TNBC have recently been revealed. Re‐expression of the silenced miRNAs miR‐17‐5p and miR‐3178 in TNBC inhibited cell proliferation and migration by targeting ETV1 and NOTCH1, respectively 34,35 . In addition, miR‐185 suppressed tumour proliferation by directly downregulating E2F6 and DNMT1, thus indirectly upregulating BRCA1 in TNBC 36 …”

Section: Micrornasmentioning

confidence: 99%

Systematic characterization of non‐coding RNAs in triple‐negative breast cancer

et al. 2020

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Triple‐negative breast cancer (TNBC) is one of the most aggressive subtypes of breast cancer with negativity for oestrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor (HER2). Non‐coding RNAs (ncRNAs) make up most of the transcriptome and are widely present in eukaryotic cells. In recent years, emerging evidence suggests that ncRNAs, mainly microRNAs (miRNAs), long ncRNAs (lncRNAs) and circular RNAs (circRNAs), play prominent roles in the tumorigenesis and development of TNBC, but the functions of most ncRNAs have not been fully described. In this review, we systematically elucidate the general characteristics and biogenesis of miRNAs, lncRNAs and circRNAs, discuss the emerging functions of these ncRNAs in TNBC and present future perspectives in clinical practice.

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miR-3178 inhibits cell proliferation and metastasis by targeting Notch1 in triple-negative breast cancer

Cited by 48 publications

References 51 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>

microRNAs Orchestrate Pathophysiology of Breast Cancer Brain Metastasis: Advances in Therapy

Systematic characterization of non‐coding RNAs in triple‐negative breast cancer

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