Identifying microRNAs regulating B7-H3 in breast cancer: the clinical impact of microRNA-29c

Nygren, Marit Kveine; Tekle, Christina; Ingebrigtsen, Vibeke Anett; Mäkelä, Rami; Krohn, Marit; Aure, Miriam Ragle; Nunes‐Xavier, Caroline E.; Perälä, Merja; Tramm, Trine; Alsner, Jan; Overgaard, Jens; Nesland, Jahn M.; Borgen, Elin; Børresen‐Dale, Anne‐Lise; Fodstad, Øystein; Sahlberg, Kristine Kleivi; Leivonen, Suvi‐Katri

doi:10.1038/bjc.2014.113

Cited by 108 publications

(90 citation statements)

References 52 publications

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“…Both the studies of Pan et al (11) and Ohlsson Teague et al (12) revealed that miR-29c was differentially expressed in the eutopic and ectopic endometrium. miR-29c belongs to the miR-29 family, and it has been suggested to be downregulated in certain types of cancer (13)(14)(15)(16). In the present study, the expression levels of the miR-29 family in the endometrium samples from women without endometriosis, as well as in paired ectopic and eutopic endometrial tissue samples from patients with endometriosis were examined by RT-qPCR.…”

Section: Discussionmentioning

confidence: 92%

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

Long

Wan

et al. 2015

International Journal of Molecular Medicine

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Abstract. Endometriosis is a prevalent and complex gynecological disease which affects 10% of women of reproductive age. Certain studies have suggested that a substantial number of microRNAs (miRNAs or miRs) are aberrantly or differentially expressed in the ectopic endometrium. To date, to the best of our knowlewdge, there is no report available on the role of miR-29 in the endometrium. In this study, we investigated the expression of the miR-29 family in the endometrium samples from women without endometriosis, as well as in paired ectopic and eutopic endometrium samples by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results revealed that miR-29c was differentially expressed in the paired eutopic and ectopic endometrium samples. In addition, c-Jun was differentially expressed in the ectopic and eutopic endometrial tissues as determined by western blot analysis. Furthermore, the role of miR-29c in endometrial cell proliferation, invasion and apoptosis was examined in vitro. The results revealed that miR-29c exerted its effects on endometrial cells by suppressing cell proliferation and invasion, as well as promoting cell apoptosis. Furthermore, it was found that c-Jun was a novel target of miR-29c, and c-Jun reversed the effects of miR-29c on the proliferation, invasion and apoptosis of endometrial cells. To the best of our knowledge, this study is the first to identify miR-29c as a suppressor of endometriosis. Taken together, our results suggest that miR-29c exerts its effects on endometrial cell proliferation, apoptosis and invasion by inhibiting the expression of c-Jun. Our data may provide a novel potential therapeutic target for the treatment of endometriosis.

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Section: Discussionmentioning

confidence: 92%

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

Long

Wan

et al. 2015

International Journal of Molecular Medicine

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“…Additionally, high levels of hsa-miR-342-5p [72, 73] and -34a [74, 75] have been correlated to breast cancer decreased recurrence and increased survival; whereas low levels have been associated with cell death inhibition and therapy resistance. The hsa-miR-22 [76, 77] and members of the hsa-miR-29 family (-29a, -29b and -29c) [55, 78] – previously identified as tumour suppressors – have also been implicated in increased survival [78] and pointed out as promising prognostic biomarkers [77, 79]. …”

Section: Discussionmentioning

confidence: 99%

Basal-like breast cancer: molecular profiles, clinical features and survival outcomes

et al. 2017

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BackgroundBasal-like constitutes an important molecular subtype of breast cancer characterised by an aggressive behaviour and a limited therapy response. The outcome of patients within this subtype is, however, divergent. Some individuals show an increased risk of dying in the first five years, and others a long-term survival of over ten years after the diagnosis. In this study, we aim at identifying markers associated with basal-like patients’ survival and characterising subgroups with distinct disease outcome.MethodsWe explored the genomic and transcriptomic profiles of 351 basal-like samples from the METABRIC and ROCK data sets. Two selection methods, labelled Differential and Survival filters, were employed to determine genes/probes that are differentially expressed in tumour and control samples, and are associated with overall survival. These probes were further used to define molecular subgroups, which vary at the microRNA level and in DNA copy number.ResultsWe identified the expression signature of 80 probes that distinguishes between two basal-like subgroups with distinct clinical features and survival outcomes. Genes included in this list have been mainly linked to cancer immune response, epithelial-mesenchymal transition and cell cycle. In particular, high levels of CXCR6, HCST, C3AR1 and FPR3 were found in Basal I; whereas HJURP, RRP12 and DNMT3B appeared over-expressed in Basal II. These genes exhibited the highest betweenness centrality and node degree values and play a key role in the basal-like breast cancer differentiation. Further molecular analysis revealed 17 miRNAs correlated to the subgroups, including hsa-miR-342-5p, -150, -155, -200c and -17. Additionally, increased percentages of gains/amplifications were detected on chromosomes 1q, 3q, 8q, 10p and 17q, and losses/deletions on 4q, 5q, 8p and X, associated with reduced survival.ConclusionsThe proposed signature supports the existence of at least two subgroups of basal-like breast cancers with distinct disease outcome. The identification of patients at a low risk may impact the clinical decisions-making by reducing the prescription of high-dose chemotherapy and, consequently, avoiding adverse effects. The recognition of other aggressive features within this subtype may be also critical for improving individual care and for delineating more effective therapies for patients at high risk.Electronic supplementary materialThe online version of this article (doi:10.1186/s12920-017-0250-9) contains supplementary material, which is available to authorized users.

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“…Our observations extended earlier reports on the role of these miRNAs in BC. [22][23][24][25][26] Previous reports on miRNAs in BC included studies on the plasma level of miRNAs miR-210, miR-21, miR-29a, and miR-126, 10b using real-time PCR. 22,23 They found plasma miR-210, 10b levels to be higher in patients with BC, which is in agreement with our study.…”

Section: Discussionmentioning

confidence: 99%

Breast tissue–based microRNA panel highlights microRNA-23a and selected target genes as putative biomarkers for breast cancer

Eissa¹,

Matboli²,

Shehata³

2015

Translational Research

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Identifying microRNAs regulating B7-H3 in breast cancer: the clinical impact of microRNA-29c

Cited by 108 publications

References 52 publications

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun

Basal-like breast cancer: molecular profiles, clinical features and survival outcomes

Breast tissue–based microRNA panel highlights microRNA-23a and selected target genes as putative biomarkers for breast cancer

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