MicroRNA expression profiling of human breast cancer identifies new markers of tumor subtype

Blenkiron, Cherie; Goldstein, Leonard D.; Thorne, Natalie; Spiteri, Inmaculada; Chin, Suet-Feung; Dunning, Mark J.; Barbosa‐Morais, Nuno L.; Teschendorff, Andrew E.; Green, Andrew; Ellis, Ian O.; Tavaré, Simon; Caldas, Carlos; Miska, Eric A.

doi:10.1186/gb-2007-8-10-r214

Cited by 868 publications

(851 citation statements)

References 115 publications

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“…In cell culture models, miR-205, along with the miR-200 family, suppresses the expression of ZEB1 and ZEB2, repressors of E-cadherin transcription that have been implicated in epithelialmesenchymal transition. 60 Downregulation of miR-205 is also seen in epithelial-mesenchymal transition induced by mammosphere culture of breast cancer cell line MCF-7. 78 Interestingly, expression of miR-205 is downregulated in breast cancer cell lines that belong to claudin-low subtype, which is known to be associated with high epithelial-mesenchymal transition, 79 as well as in triple-negative breast cancer human samples.…”

Section: Discussionmentioning

confidence: 99%

“…More important than its feasibility, recent advances have implicated the role of miRNA as oncogenes or tumor suppressor genes in tumorigenesis, metastasis, and response to treatment in various cancer types including breast cancer. [18][19][20][21][22][23][24][25][26][27] Although the number of miRNAs identified is relatively small (∼2588 human mature miRNAs from 1881 precusor miRNA genes reported in miRBASEv.21; www.mirbase.org), individual miRNAs can target multiple genes, and it is thought that collectively they can target approximately onethird of the human genes. 28 Thus, they act as global regulators and may be suitable diagnostic markers and therapeutic targets for inflammatory breast cancer.…”

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confidence: 99%

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MicroRNA expression profiling identifies decreased expression of miR-205 in inflammatory breast cancer

et al. 2016

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Inflammatory breast cancer is the most aggressive form of breast cancer. Identifying new biomarkers to be used as therapeutic targets is in urgent need. Messenger RNA expression profiling studies have indicated that inflammatory breast cancer is a transcriptionally heterogeneous disease, and specific molecular targets for inflammatory breast cancer have not been well established. We performed microRNA expression profiling in inflammatory breast cancer in comparison with locally advanced noninflammatory breast cancer in this study. Although many microRNAs were differentially expressed between normal breast tissue and tumor tissue, most of them did not show differential expression between inflammatory and noninflammatory tumor samples. However, by microarray analysis, quantitative reverse transcription PCR, and in situ hybridization, we showed that microRNA-205 expression was decreased not only in tumor compared with normal breast tissue, but also in inflammatory breast cancer compared with noninflammatory breast cancer. Lower expression of microRNA-205 correlated with worse distant metastasis-free survival and overall survival in our cohort. A small-scale immunohistochemistry analysis showed coexistence of decreased microRNA-205 expression and decreased E-cadherin expression in some ductal tumors. MicroRNA-205 may serve as a therapeutic target in advanced breast cancer including inflammatory breast cancer.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

MicroRNA expression profiling identifies decreased expression of miR-205 in inflammatory breast cancer

et al. 2016

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“…This would be in keeping with multiple other studies showing dysregulation of parts of the pathway in cancer cell lines and tissues. 37,38 It is likely that there is a complex interaction between microRNA processing machinery, already abnormal in cancer cells, 39 and microRNA induced in hypoxia. It may also reflect post-translational processes such as prolyl 4-hydroxylation: the same process that regulates von Hippel-Lindau gene, and in turn HIFm, regulates Argonaute 2 stability.…”

Section: Discussionmentioning

confidence: 99%

hsa‐miR‐210 is a marker of tumor hypoxia and a prognostic factor in head and neck cancer

Gee

Camps

Buffa

et al. 2010

Cancer

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BACKGROUND:Hypoxia is an important mechanism of treatment resistance in head and neck squamous cell carcinoma (HNSCC). MicroRNAs are short noncoding RNAs that regulate multiple mRNAs and are frequently dysregulated in cancer. The authors have investigated the role of 3 microRNAs, including the hypoxia-induced hsa-miR-210, as potential markers of hypoxia or prognosis. METHODS: Three hypoxia-related microRNAs, hsa-miR-210, hsa-miR-21, and hsa-miR-10b, were measured in 46 samples from patients with HNSCC. Expression levels were correlated with clinicopathological variables and other markers of hypoxia: a published 99-gene hypoxia metagene, individual hypoxia-related genes such as TWIST1, and immunohistochemical expression of hypoxia-inducible factor 1 and its target gene carbonic anhydrase 9. We then performed survival analyses to investigate the prognostic significance of these microRNAs. RESULTS: Only the level of hsa-miR-210 was significantly correlated with other markers of hypoxia, including the 99-gene hypoxia metagene (rho ¼ 0.67, P < .001). We found no association between hsa-miR-210, hsamiR-21, or hsa-miR-10b and clinicopathological variables such as tumor size, differentiation, and stage. However, high levels of hsa-miR-210 were associated with locoregional disease recurrence (P ¼ .001) and short overall survival (P ¼ .008). hsa-miR-21 and hsa-miR-10b had no prognostic significance. CONCLUSIONS: Expression of hsa-miR-210 in head and neck cancer correlates with other approaches for assessing hypoxia and is associated with prognosis. This warrants further study as a classification marker of patients for therapies involving modulation of hypoxia.

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“…Interestingly, in solid tumors, such as prostate, colon, stomach, pancreas, lung and breast, the spectrum of miRNAs expressed (miRNome) is different from that of the corresponding normal tissues (Volinia et al, 2006), suggesting the involvement of miRNAs in transformed cell biology. Differential expression of miRNA genes was found associated with specific pathological features of BC, where distinct miRNA expression profiles in normal vs cancer tissue or between different molecular and clinical tumor subtypes appears to be the rule (Iorio et al, 2005;Lu et al, 2005;Blenkiron et al, 2007;Tavazoie et al, 2008). There is increasing evidence, in fact, that specific miRNAs may be responsible at large for disease heterogeneity, functioning as regulators of tumorigenicity, invasion and metastasis (Tavazoie et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Direct regulation of microRNA biogenesis and expression by estrogen receptor beta in hormone-responsive breast cancer

et al. 2012

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Estrogen effects on mammary epithelial and breast cancer (BC) cells are mediated by the nuclear receptors ERa and ERb, transcription factors that display functional antagonism with each other, with ERb acting as oncosuppressor and interfering with the effects of ERa on cell proliferation, tumor promotion and progression. Indeed, hormone-responsive, ERa þ BC cells often lack ERb, which when present associates with a less aggressive clinical phenotype of the disease. Recent evidences point to a significant role of microRNAs (miRNAs) in BC, where specific miRNA expression profiles associate with distinct clinical and biological phenotypes of the lesion. Considering the possibility that ERb might influence BC cell behavior via miRNAs, we compared miRNome expression in ERb þ vs ERbÀ hormone-responsive BC cells and found a widespread effect of this ER subtype on the expression pattern of these non-coding RNAs. More importantly, the expression pattern of 67 miRNAs, including 10 regulated by ERb in BC cells, clearly distinguishes ERb þ , node-negative, from ERbÀ, metastatic, mammary tumors. Molecular dissection of miRNA biogenesis revealed multiple mechanisms for direct regulation of this process by ERb þ in BC cell nuclei. In particular, ERb downregulates miR-30a by binding to two specific sites proximal to the gene and thereby inhibiting pri-miR synthesis. On the other hand, the receptor promotes miR-23b, -27b and 24-1 accumulation in the cell by binding in close proximity of the corresponding gene cluster and preventing in situ the inhibitory effects of ERa on pri-miR maturation by the p68/DDX5-Drosha microprocessor complex. These results indicate that cell autonomous regulation of miRNA expression is part of the mechanism of action of ERb in BC cells and could contribute to establishment or maintenance of a less aggressive tumor phenotype mediated by this nuclear receptor.

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MicroRNA expression profiling of human breast cancer identifies new markers of tumor subtype

Cited by 868 publications

References 115 publications

MicroRNA expression profiling identifies decreased expression of miR-205 in inflammatory breast cancer

MicroRNA expression profiling identifies decreased expression of miR-205 in inflammatory breast cancer

hsa‐miR‐210 is a marker of tumor hypoxia and a prognostic factor in head and neck cancer

Direct regulation of microRNA biogenesis and expression by estrogen receptor beta in hormone-responsive breast cancer

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