A putative role for microRNA-205 in mammary epithelial cell progenitors

Greene, Stephanie; Gunaratne, Preethi H.; Hammond, Scott M.; Rosen, Jeffrey M.

doi:10.1242/jcs.056812

Cited by 124 publications

(89 citation statements)

References 68 publications

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“…Importantly, our study is supportive of acting as a tumor suppressor (see for example [13], but also as an oncogene that favors cell proliferation [20] or represses cell death (this study). Consequently, the use of miR-205 as a curative miRNA in cancer, as previously suggested by others [12], should be approached with great caution.…”

Section: Acinus Formation Assayssupporting

confidence: 66%

“…E-cadherin is a tumor suppressor that negatively regulates the levels of free beta-catenin, thereby controlling cell proliferation [21] as well as the formation of adherens junctions [22]. In MCF10 cells, the expression of Given that the larger acinus structure might be due to an increase in cell proliferation, as was previously shown in a different cell line [20], we next assessed the proliferation rate of MCF10A-205. Surprisingly, miR-205 overexpression did not alter the proliferation of MCF10A cells, whether in two-dimensional (as assessed using the WST1 assay, Figure 5A) or in threedimensional cultures (as monitored by Ki67 staining, Figure 5B).…”

Section: Resultsmentioning

confidence: 99%

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Mir-205 modulates acinar size and morphology of transformed breast epithelial cells

Neri¹,

Beldiman²,

Brouard³

et al. 2012

OncomiRs

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In 3D cultures, breast epithelial cells form lobular acini that structurally resemble breast alveoli in vivo. Enlarged acini with modified acinar morphology are characteristic of transformed and/or cancer breast cells. A genome-wide miRNA expression screen comparing non-transformed and tumorigenic MCF10A cell lines identified miR-205 as a potential modifier of acinus size. In support of this hypothesis, miR-205 was found overexpressed in transformed and tumorigenic MCF10 cells. We showed that forced expression of miR-205 in non-transformed MCF10A cells increased the size of acini, whereas miR-205 antisense oligonucleotides restored a normal morphology. MiR-205 did not modify cell proliferation but rather inhibited apoptotic cell death. Moreover, miR-205 targets ZEB1, an inhibitor of E-cadherin. E-cadherin was induced upon miR-205 overexpression. Downregulating E-cadherin restored normal acinar morphology in miR-205 expressing cells, consistent with E-cadherin being involved in the miR-205-dependent acini phenotype.

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Section: Acinus Formation Assayssupporting

confidence: 66%

Section: Resultsmentioning

confidence: 99%

Mir-205 modulates acinar size and morphology of transformed breast epithelial cells

Neri¹,

Beldiman²,

Brouard³

et al. 2012

OncomiRs

View full text Add to dashboard Cite

show abstract

“…67 In addition, high expression of miR-205 has been observed in stem cell-enriched populations of normal mouse mammary epithelial cells isolated by FACS purification. 68 Thus, miR-205 may play a role in mammary epithelial stem cell proliferation and differentiation. Its functions in cancer appear to be tissue type specific.…”

Section: Discussionmentioning

confidence: 99%

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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“…Compared to their role in ESCs, there is less evidence for the involvement of miRNAs in the self-renewal of somatic stem cells. The overexpression of miR-205 enhanced proliferation and expanded the population of progenitor cells by modulating PTEN, a tumor-suppressor gene [46] . Therefore, stem cell self-renewal is tightly regulated through a complex network of core transcription factors, miRNAs, and the repression and/or promotion of differentiation mechanisms and pluripotent pathways, respectively ( Figure 1).…”

Section: Micrornas In Maintenancementioning

confidence: 99%

MicroRNAs as novel regulators of stem cell fate

Choi

Hwang³

2013

WJSC

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Mounting evidence in stem cell biology has shown that microRNAs (miRNAs) play a crucial role in cell fate specification, including stem cell self-renewal, lineagespecific differentiation, and somatic cell reprogramming. These functions are tightly regulated by specific gene expression patterns that involve miRNAs and transcription factors. To maintain stem cell pluripotency, specific miRNAs suppress transcription factors that promote differentiation, whereas to initiate differentiation, lineagespecific miRNAs are upregulated via the inhibition of transcription factors that promote self-renewal. Small molecules can be used in a similar manner as natural miRNAs, and a number of natural and synthetic small molecules have been isolated and developed to regulate stem cell fate. Using miRNAs as novel regulators of stem cell fate will provide insight into stem cell biology and aid in understanding the molecular mechanisms and crosstalk between miRNAs and stem cells.Ultimately, advances in the regulation of stem cell fate will contribute to the development of effective medical therapies for tissue repair and regeneration. This review summarizes the current insights into stem cell fate determination by miRNAs with a focus on stem cell self-renewal, differentiation, and reprogramming. Small molecules that control stem cell fate are also highlighted.© 2013 Baishideng. All rights reserved. Key words:MicroRNA; Stem cell fate; Differentiation; Self-renewal; Reprogramming; Small molecule Core tip: Stem cells are important in regenerative medicine applications due to their capacity to self-renew and differentiate into specific cell types. MicroRNAs (miRNAs) are short non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. Recent studies suggest that miRNAs are key molecules in the regulation of stem cell fate decisions; this regulation is manifested as the fine tuning of cell-and tissue-specific gene expression. This review summarizes the current insights into stem cell fate determination by miRNAs and focuses on stem cell self-renewal, differentiation, and reprogramming. Small molecules that control stem cell fate are also highlighted.

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A putative role for microRNA-205 in mammary epithelial cell progenitors

Cited by 124 publications

References 68 publications

Mir-205 modulates acinar size and morphology of transformed breast epithelial cells

Mir-205 modulates acinar size and morphology of transformed breast epithelial cells

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

MicroRNAs as novel regulators of stem cell fate

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