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Journal ArticleDOI

MicroRNA in prostate, bladder, and kidney cancer: a systematic review.

TL;DR: MiRNAs appear to be important modulators of urologic cancer, and many are functionally implicated in their pathogenesis.
About: This article is published in European Urology.The article was published on 2011-05-01. It has received 448 citations till now. The article focuses on the topics: Cancer & Gene silencing.
Citations
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01 Jan 2009
TL;DR: In this article, a review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.
Abstract: MicroRNAs (miRNAs) are endogenous ∼23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.

646 citations

Journal ArticleDOI
TL;DR: Observations suggest that changes in miR concentration in prostate cancer patients may be identified by analysing various body fluids, and circulating miRs may be used to diagnose and stage prostate cancer.
Abstract: BACKGROUND: The aim of this study was to investigate the hypothesis that changes in circulating microRNAs (miRs) represent potentially useful biomarkers for the diagnosis, staging and prediction of outcome in prostate cancer. METHODS: Real-time polymerase chain reaction analysis of 742 miRs was performed using plasma-derived circulating microvesicles of 78 prostate cancer patients and 28 normal control individuals to identify differentially quantified miRs. RESULTS: A total of 11 miRs were differentially quantified in prostate cancer patients compared with controls, including 9 in patients without metastases. In all, 16 miRs were present in significantly greater amounts in prostate cancer patients with metastases compared with those without metastases. The association of miR-141 and miR-375 with metastatic prostate cancer was confirmed using serum-derived exosomes and microvesicles in a separate cohort of patients with recurrent or non-recurrent disease following radical prostatectomy. An analysis of five selected miRs in urine samples found that miR-107 and miR-574-3p were quantified at significantly higher concentrations in the urine of men with prostate cancer compared with controls. CONCLUSION: These observations suggest that changes in miR concentration in prostate cancer patients may be identified by analysing various body fluids. Moreover, circulating miRs may be used to diagnose and stage prostate cancer.

645 citations


Cites background from "MicroRNA in prostate, bladder, and ..."

  • ...Several miRs have altered function or are differentially present in prostate cancer (Catto et al, 2011)....

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Journal ArticleDOI
TL;DR: It is hypothesized that reversible epigenetic events regulate both EMT and MET, and thus, also regulate the development of different types of metastatic cancers.
Abstract: EMT and MET comprise the processes by which cells transit between epithelial and mesenchymal states, and they play integral roles in both normal development and cancer metastasis. This article reviews these processes and the molecular pathways that contribute to them. First, we compare embryogenesis and development with cancer metastasis. We then discuss the signaling pathways and the differential expression and down-regulation of receptors in both tumor cells and stromal cells, which play a role in EMT and metastasis. We further delve into the clinical implications of EMT and MET in several types of tumors, and lastly, we discuss the role of epigenetic events that regulate EMT/MET processes. We hypothesize that reversible epigenetic events regulate both EMT and MET, and thus, also regulate the development of different types of metastatic cancers.

601 citations


Additional excerpts

  • ...6% Snail, Twist, Zeb1, Zeb2, E-cadherin, CCR7, Claudin-1, Fibronectin, Klf8, miR-9, miR-34, miR-200, N-cadherin, Occludin, PTEN, Slug, STK11, [62,63,66,72,79-82]...

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  • ...4% TGF-β, BMP-7, Claudin-1, HDAC1,2,3, hepatocyte growth factor, Klf8, miR-23b, miR-29b, miR-34, miRs-141/200, miR-205, miR-438-3p, [62,66,72-74]...

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  • ...7% Snail, Twist, vimentin, Zeb1, Zeb2, β-catenin, Brachyury, CD44, E-cadherin, EZH2 FGFR4, Fibronectin, HDAC1,2,3, LSD1, miR-34, p16, SIRT1, Slug, SUZ12, SUV39H1, [62,63,66,72]...

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  • ...Table 1 Major tumor types organized by virulence, clinical significance, and epigenetic markers Cancer type Survival 5-years after cancer has metastasized [61] Survival 5-years after diagnosis [61] EMT Markers References Pancreas 2.3% 6.7% Snail, Twist, Zeb1, Zeb2, E-cadherin, β-catenin Brachyury, HDAC1,2,3, miR-34, miR-200, [62-65] Liver 2.8% 16.6% Snail, Twist, Zeb1, Zeb2, TGF-β, EZH2, HDAC1,2,3, miR-101, STAT3, SUZ12, [62,66,67] Lung 4.0% 16.8% Snail, Zeb1, Zeb2, E-cadherin, vimentin, α-catenin, EZH2, BMI1, Brachyury, Claudin-1, Cytokeratins, G9a, HDAC1,2,3, LSD1, miR-34, miR-101, miR-205, Periostin, Slug, SUZ12, TTF-1, versican, N-cadherin [62,63,66,68-71] Bladder 5.5% 77.4% Twist, Zeb1, Zeb2, N-cadherin, EZH2, Fibronectin, LSD1, miRs-1/133a/218, miR-19a, miRs-30a-3p/133a/199a, miR-34, miR-99a/100, miR-101, miR-125b, miR-129, miR-145/133a, miR-200, miR-205, miR-221, N- [62,66,72] Renal 12.1% 72.4% TGF-β, BMP-7, Claudin-1, HDAC1,2,3, hepatocyte growth factor, Klf8, miR-23b, miR-29b, miR-34, miRs-141/200, miR-205, miR-438-3p, [62,66,72-74] Colorectal 12.9% 64.7% Snail, Twist, vimentin, Zeb1, Zeb2, β-catenin, Brachyury, CD44, E-cadherin, EZH2, FGFR4, Fibronectin, HDAC1,2,3, LSD1, miR-34, p16INK4a, SIRT1, Slug, SUZ12, SUV39H1, [62,63,66,72] Cervical 16.1% 67.9% Snail, Twist, E-cadherin, vimentin, β-catenin, EGFR, [63,66,75,76] Skin melanoma 16.1% 91.3% TGF-β, MITF, N-cadherin, miR-205 [62,77,78] Ovarian 27.4% 44.6% Snail, Twist, Zeb1, Zeb2, E-cadherin, CCR7, Claudin-1, Fibronectin, Klf8, miR-9, miR-34, miR-200, N-cadherin, Occludin, PTEN, Slug, STK11, [62,63,66,72,79-82] Breast 25.0% 89.2% Snail, Zeb1, Zeb2, vimentin, β-catenin, E-cadherin, BMI1, Brachyury, Claudin, EZH2, HDAC1,2,3, Klf8, LSD1, miR-9 (2); miR-10b, miR-34, Slug, SUZ12, Twist, versican, [62,63,66,68,69,83,84] Prostate 28.0% 98.9% Twist, Zeb1, N-cadherin, APC, Cyclin D2, collagen, decorin, E47, E-cadherin, ER, EZH2, Fibronectin, GSTP1, HDAC1,2,3, Let-7a, LSD1, miR-1, miR-7, miR-15a-16 cluster, miR20a, miR-21, miR-24, miR-32, miR-34a, miR-34c, miR-101, miR-106b, miR-107, miR125b, miR-143, miR-145, miR-146a, miR-148a, miR-205, miR-221, miR-222, miR-331-3P, miR-449a, miR-521, miR-1296, Notch-1, RAR-β2, RASSF1A, versican, [62,63,72,85-88] Brain/nervous system 35.6% 33.4% miR-9, Klf8 [62] H eerboth et al.Clinicaland TranslationalM edicine (2015) 4:6 Page 5 of 13...

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  • ...9% Twist, Zeb1, N-cadherin, APC, Cyclin D2, collagen, decorin, E47, E-cadherin, ER, EZH2, Fibronectin, GSTP1, HDAC1,2,3, Let-7a, LSD1, miR-1, miR-7, miR-15a-16 cluster, miR20a, miR-21, miR-24, miR-32, miR-34a, miR-34c, miR-101, miR-106b, miR-107, miR125b, miR-143, miR-145, miR-146a, miR-148a, miR-205, miR-221, miR-222, miR-331-3P, miR-449a, miR-521, miR-1296, Notch-1, RAR-β2, RASSF1A, versican, [62,63,72,85-88]...

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Journal ArticleDOI
TL;DR: It is shown that circHIPK3, also named bladder cancer‐related circular RNA‐2 (BCRC‐2), is significantly down‐regulated in bladder cancer tissues and cell lines, and negatively correlates with bladder cancer grade, invasion as well as lymph node metastasis, respectively.
Abstract: Increasing evidences suggest that circular RNAs (circRNAs) exert crucial functions in regulating gene expression. In this study, we perform RNA‐seq and identify 6,154 distinct circRNAs from human bladder cancer and normal bladder tissues. We find that hundreds of circRNAs are significantly dysregulated in human bladder cancer tissues. We further show that circHIPK3, also named bladder cancer‐related circular RNA‐2 (BCRC‐2), is significantly down‐regulated in bladder cancer tissues and cell lines, and negatively correlates with bladder cancer grade, invasion as well as lymph node metastasis, respectively. Over‐expression of circHIPK3 effectively inhibits migration, invasion, and angiogenesis of bladder cancer cells in vitro and suppresses bladder cancer growth and metastasis in vivo . Mechanistic studies reveal that circHIPK3 contains two critical binding sites for the microRNA miR‐558 and can abundantly sponge miR‐558 to suppress the expression of heparanase (HPSE). Taken together, our findings provide evidence that circRNAs act as “microRNA sponges”, and suggest a new therapeutic target for the treatment of bladder cancer.

442 citations


Cites background from "MicroRNA in prostate, bladder, and ..."

  • ...Increasing evidence suggests that miRNAs are aberrantly expressed in bladder cancer, and exert multiple influences on promoting or inhibiting carcinogenesis, development, apoptosis, invasion, and metastasis [23,24]....

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Journal ArticleDOI
TL;DR: It is found that metformin significantly decreased cell survival, clonogenicity, wound-healing capacity, sphere-forming capacity (pancreatospheres), and increased disintegration of pancreatospheres in both gemcitabine-sensitive and gemcitABine-resistant pancreatic cancer cells.
Abstract: Pancreatic cancer is the fourth leading cause of cancer-related deaths in the United States, which is, in part, due to intrinsic (de novo) and extrinsic (acquired) resistance to conventional therapeutics, suggesting that innovative treatment strategies are required for overcoming therapeutic resistance to improve overall survival of patients. Oral administration of metformin in patients with diabetes mellitus has been reported to be associated with reduced risk of pancreatic cancer and that metformin has been reported to kill cancer stem cells (CSC); however, the exact molecular mechanism(s) has not been fully elucidated. In the current study, we examined the effect of metformin on cell proliferation, cell migration and invasion, and self-renewal capacity of CSCs and further assessed the expression of CSC marker genes and microRNAs (miRNA) in human pancreatic cancer cells. We found that metformin significantly decreased cell survival, clonogenicity, wound-healing capacity, sphere-forming capacity (pancreatospheres), and increased disintegration of pancreatospheres in both gemcitabine-sensitive and gemcitabine-resistant pancreatic cancer cells. Metformin also decreased the expression of CSC markers,CD44, EpCAM,EZH2, Notch-1, Nanog and Oct4, and caused reexpression of miRNAs (let-7a,let-7b, miR-26a, miR-101, miR-200b, and miR-200c) that are typically lost in pancreatic cancer and especially in pancreatospheres. We also found that reexpression of miR-26a by transfection led to decreased expression of EZH2 and EpCAM in pancreatic cancer cells. These results clearly suggest that the biologic effects of metformin are mediated through reexpression of miRNAs and decreased expression of CSC-specific genes, suggesting that metformin could be useful for overcoming therapeutic resistance of pancreatic cancer cells.

325 citations


Cites background from "MicroRNA in prostate, bladder, and ..."

  • ...In the pathogenesis of cancer, let-7 family of miRNAs has been found to be downregulated, thereby increasing the expression of Ras and c-Myc inmalignant cells (40, 42, 43)....

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References
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Journal ArticleDOI
23 Jan 2009-Cell
TL;DR: The current understanding of miRNA target recognition in animals is outlined and the widespread impact of miRNAs on both the expression and evolution of protein-coding genes is discussed.

18,036 citations


"MicroRNA in prostate, bladder, and ..." refers background in this paper

  • ...This preservation in primitive species points to their importance in cell function and led to the current interest in their function [2]....

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  • ...The affinity of this bond depends on the sequence and number of complementary seeds [2]....

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  • ...Most miRNAs produce a modest reduction (less than twofold) in their target mRNA concentration (to ‘‘fine-tune’’ protein expression) [2]....

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Journal ArticleDOI
TL;DR: It is shown here that miRNAs are present in human plasma in a remarkably stable form that is protected from endogenous RNase activity and established the measurement of tumor-derived mi RNAs in serum or plasma as an important approach for the blood-based detection of human cancer.
Abstract: Improved approaches for the detection of common epithelial malignancies are urgently needed to reduce the worldwide morbidity and mortality caused by cancer. MicroRNAs (miRNAs) are small (≈22 nt) regulatory RNAs that are frequently dysregulated in cancer and have shown promise as tissue-based markers for cancer classification and prognostication. We show here that miRNAs are present in human plasma in a remarkably stable form that is protected from endogenous RNase activity. miRNAs originating from human prostate cancer xenografts enter the circulation, are readily measured in plasma, and can robustly distinguish xenografted mice from controls. This concept extends to cancer in humans, where serum levels of miR-141 (a miRNA expressed in prostate cancer) can distinguish patients with prostate cancer from healthy controls. Our results establish the measurement of tumor-derived miRNAs in serum or plasma as an important approach for the blood-based detection of human cancer.

7,296 citations


"MicroRNA in prostate, bladder, and ..." refers background in this paper

  • ...As discussed later, miR-141 is upregulated in human PCa [38]....

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  • ...For example, MiR-141 is upregulated in primary PCa and was found to be detectable in circulating serum from affected patients [38]....

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Journal ArticleDOI
09 Jun 2005-Nature
TL;DR: It is found that the levels of the primary or mature microRNAs derived from the mir-17–92 locus are often substantially increased in human B-cell lymphomas, and the cluster is implicate as a potential human oncogene.
Abstract: To date, more than 200 microRNAs have been described in humans; however, the precise functions of these regulatory, non-coding RNAs remains largely obscure. One cluster of microRNAs, the mir-17-92 polycistron, is located in a region of DNA that is amplified in human B-cell lymphomas. Here we compared B-cell lymphoma samples and cell lines to normal tissues, and found that the levels of the primary or mature microRNAs derived from the mir-17-92 locus are often substantially increased in these cancers. Enforced expression of the mir-17-92 cluster acted with c-myc expression to accelerate tumour development in a mouse B-cell lymphoma model. Tumours derived from haematopoietic stem cells expressing a subset of the mir-17-92 cluster and c-myc could be distinguished by an absence of apoptosis that was otherwise prevalent in c-myc-induced lymphomas. Together, these studies indicate that non-coding RNAs, specifically microRNAs, can modulate tumour formation, and implicate the mir-17-92 cluster as a potential human oncogene.

3,735 citations


"MicroRNA in prostate, bladder, and ..." refers background in this paper

  • ...For example, the oncogene MYC transcriptionally activates the miR-17-92 cluster on chromosome 13 to initiate carcinogenesis [14]....

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01 Jun 2010
TL;DR: Results show that changes in mRNA levels closely reflect the impact of miRNAs on gene expression and indicate that destabilization of target mRNAs is the predominant reason for reduced protein output.
Abstract: MicroRNAs (miRNAs) are endogenous approximately 22-nucleotide RNAs that mediate important gene-regulatory events by pairing to the mRNAs of protein-coding genes to direct their repression. Repression of these regulatory targets leads to decreased translational efficiency and/or decreased mRNA levels, but the relative contributions of these two outcomes have been largely unknown, particularly for endogenous targets expressed at low-to-moderate levels. Here, we use ribosome profiling to measure the overall effects on protein production and compare these to simultaneously measured effects on mRNA levels. For both ectopic and endogenous miRNA regulatory interactions, lowered mRNA levels account for most (>/=84%) of the decreased protein production. These results show that changes in mRNA levels closely reflect the impact of miRNAs on gene expression and indicate that destabilization of target mRNAs is the predominant reason for reduced protein output.

3,444 citations


"MicroRNA in prostate, bladder, and ..." refers background in this paper

  • ...A small proportion causes upregulation, or the complete destruction of their target [2–4]....

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Journal ArticleDOI
12 Aug 2010-Nature
TL;DR: In this paper, the authors used ribosome profiling to measure the overall effects on protein production and compare these to simultaneously measured effects on mRNA levels, showing that changes in mRNA levels closely reflect the impact of miRNAs on gene expression and indicate that destabilization of target mRNAs is the predominant reason for reduced protein output.
Abstract: MicroRNAs (miRNAs) are endogenous approximately 22-nucleotide RNAs that mediate important gene-regulatory events by pairing to the mRNAs of protein-coding genes to direct their repression. Repression of these regulatory targets leads to decreased translational efficiency and/or decreased mRNA levels, but the relative contributions of these two outcomes have been largely unknown, particularly for endogenous targets expressed at low-to-moderate levels. Here, we use ribosome profiling to measure the overall effects on protein production and compare these to simultaneously measured effects on mRNA levels. For both ectopic and endogenous miRNA regulatory interactions, lowered mRNA levels account for most (>/=84%) of the decreased protein production. These results show that changes in mRNA levels closely reflect the impact of miRNAs on gene expression and indicate that destabilization of target mRNAs is the predominant reason for reduced protein output.

3,401 citations