RETRACTED: A Pleiotropically Acting MicroRNA, miR-31, Inhibits Breast Cancer Metastasis

Valastyan, Scott; Reinhardt, Ferenc; Benaich, Nathan; Calogrias, Diana; Szász, Attila Marcell; Wang, Zhigang C.; Brock, Jane E.; Richardson, Andrea L.; Weinberg, Robert A.

doi:10.1016/j.cell.2009.03.047

Cited by 778 publications

(732 citation statements)

References 40 publications

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“…Enforced expression of miR-409 could suppress the migration, invasion and metastasis of GC cells in vitro and in vivo. We further identified RDX, a putative pro-metastatic gene, 20,25 as a direct functional target of miR-409. To our knowledge, this is the first study to explore the role of miR-409 in cancer, and our results indicate that miR-409 acts to suppress metastasis in GC.…”

Section: Discussionmentioning

confidence: 99%

“…21 RDX was originally identified as a constituent of adherence junctions in the livers of rats, 36 and it has more recently been implicated in cancer progression and metastasis. 20,24,25,39 It has been reported that RDX may cooperate with ITGA5 and RhoA to affect three distinct steps in the invasionmetastasis cascade in vivo, local invasion, early post-intravasation events and metastatic colonisation. 25 Silencing of RDX has also been found to suppress the migration and invasion of GC cells.…”

Section: Discussionmentioning

confidence: 99%

“…20,24,25 To determine whether downregulation of RDX was involved in miR-409-mediated suppression of migration and invasion, we first analysed the effects of RDX in GC cells. As shown in Figures 6a and b, transfection of a specific small interfering RNA against RDX into SGC-7901 and HGC-27 cells led to sharply decreased RDX expression.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-409 suppresses tumour cell invasion and metastasis by directly targeting radixin in gastric cancers

et al. 2011

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Emerging evidence has shown that aberrantly expressed microRNAs (miRNAs) are highly associated with tumour development and progression. However, little is known about the potential role of miRNAs in gastric cancer (GC) metastasis. In this study, miR-409-3p was found to be downregulated frequently in human GCs, and its expression was significantly associated with tumor-node-metastasis (TNM) stage and lymph node metastasis. Enforced expression of miR-409 in GC cells significantly reduced their migration and invasion in vitro and their capacity to develop distal pulmonary metastases and peritoneal dissemination in vivo. Moreover, we found that miR-409 exerted its function predominantly through the mature miR-409-3p, but not miR-409-5p. Microarray and bioinformatics analysis identified the pro-metastatic gene radixin (RDX) as a potential miR-409-3p target. Further studies confirmed that miR-409-3p suppressed the expression of RDX by directly binding to its 3 0 -untranslated region. Silencing of RDX by small interfering RNAs phenocopied the effects of miR-409 overexpression, whereas restoration of RDX in miR-409-overexpressed GC cells reversed the suppressive effects of miR-409. Taken together, these results demonstrate that miR-409 suppresses GC cell invasion and metastasis by directly targeting RDX and that patients with downregulated miR-409-3p are prone to lymph node metastasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MicroRNA-409 suppresses tumour cell invasion and metastasis by directly targeting radixin in gastric cancers

et al. 2011

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“…17 miR-31 uses multiple mechanisms to oppose the breast cancer metastasis. 18 miR-208 regulates cardiac growth and gene expression in response to stress and hormonal signaling. 14 Autophagy is regulated by a variety of factors in which the autophagy-related genes (ATGs) control the different stages of autophagy including initiation and elongation.…”

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confidence: 99%

Autophagic program is regulated by miR-325

Fang

et al. 2014

Cell Death Differ

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Autophagy is required for the maintenance of cardiomyocytes homeostasis. However, the abnormal autophagy could lead to the development of heart failure. Autophagy is enhanced during myocardial ischemia/reperfusion; it remains to elucidate the molecular regulation of autophagy. We report here that miR-325, ARC and E2F1 constitute an axis that regulates autophagy. Our results showed that miR-325 expression is upregulated upon anoxia/reoxygenation and ischemia/reperfusion. Cardiomyocytespecific overexpression of the miR-325 potentiates autophagic responses and myocardial infarct sizes, whereas knockdown of miR-325 inhibited autophagy and cell death. We searched for the downstream mediator of miR-325 and identified that ARC is a target of miR-325. ARC transgenic mice could attenuate autophagy and myocardial infarction sizes upon pressure-overloadinduced heart failure, whereas ARC null mice exhibited an increased autophagic accumulation in the heart. The suppression of ARC by miR-325 led to its inability to repress autophagic program. In exploring the molecular mechanism by which miR-325 expression is regulated, our results revealed that the transcription factor E2F1 contributed to promote miR-325 expression. E2F1 null mice demonstrated reduced autophagy and myocardial infarction sizes upon ischemia/reperfusion. Our present study reveals a novel autophagic regulating model that is composed of E2F1, miR-325 and ARC. Modulation of their levels may provide a new approach for tackling cardiac failure.

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“…The miRNAs act as either oncogenes [13][14][15] or tumour suppressors. [16][17][18] The miRNA let-7a has been characterised as a tumour suppressor in several human cancers. [19][20][21][22][23][24] Dong et al 25 reported that let-7a is downregulated in resected prostate cancer samples and in prostate cancer cells.…”

Section: Introductionmentioning

confidence: 99%

The miRNA let-7a1 inhibits the expression of insulin-like growth factor 1 receptor (IGF1R) in prostate cancer PC-3 cells

Wang¹,

Chen²,

Zhang³

et al. 2013

Asian J Androl

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Reduced microRNA (miRNA) let-7a expression and the activation of insulin-like growth factor-1 receptor (IGF1R) signalling are both involved in prostate cancer and progression. In the present study, we demonstrated that the growth inhibitory effect of let-7a1 is directly related to targeting IGF1R gene expression in PC-3 cells. TargetScan predicted three potential target sites (T1, T2 and T3) of let-7a in the 39 untranslational region (39 UTR) of IGF1R mRNA. Real-time PCR, Western blot and luciferase reporter assays were used to detect the effects of let-7a1 overexpression or let-7a1 inhibitor on the IGF1R gene expression in PC-3 cells. The results indicated that let-7a1 could inhibit IGF1R expression by directly targeting the T1 and T2 sites in the 39 UTR of the IGF1R mRNA. We then used RT-PCR, luciferase reporter assays, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, flow cytometry and Hoechst 33342 staining to examine whether let-7a1-mediated inhibition of IGF1R expression also affects the IGF1R-mediated signalling events, including Elk1 activity and c-fos gene expression, proliferation, apoptosis and cell cycle. We demonstrated that let7a1-mediated IGF1R downregulation was accompanied by attenuation of Elk1 activity and c-fos expression, inhibition of cell proliferation, enhanced apoptosis and cell cycle arrest, and that loss function of let-7a1 via inhibition can upregulate IGF1R accompanied by an increase of Elk1 activity and c-fos expression, thereby enhancing cell proliferation. Altogether, these findings suggest that let-7a may be novel therapeutic candidate for prostate cancer.

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RETRACTED: A Pleiotropically Acting MicroRNA, miR-31, Inhibits Breast Cancer Metastasis

Cited by 778 publications

References 40 publications

MicroRNA-409 suppresses tumour cell invasion and metastasis by directly targeting radixin in gastric cancers

MicroRNA-409 suppresses tumour cell invasion and metastasis by directly targeting radixin in gastric cancers

Autophagic program is regulated by miR-325

The miRNA let-7a1 inhibits the expression of insulin-like growth factor 1 receptor (IGF1R) in prostate cancer PC-3 cells

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