Potentially important microRNA cluster on chromosome 17p13.1 in primary peritoneal carcinoma

Flavin, Richard; Smyth, Paul; Laios, Alexandros; O’Toole, Sharon; Barrett, Ciara; Finn, Stephen P.; Russell, S M; Ring, Martina; Denning, K; Li, Jinghuan; Aherne, Sinéad; Sammarae, D.; Aziz, Natasha; Alhadi, Araibi; Sheppard, B. L.; Lao, K; Sheils, Orla; O’Leary, John

doi:10.1038/modpathol.2008.135

Cited by 79 publications

(50 citation statements)

References 83 publications

(102 reference statements)

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“…In oncology reports, miR-195 has been considered as tumor suppressor and/or inhibitor of cell proliferation. miR-195 is down-regulated in tongue squamous cell carcinoma [38], primary peritoneal carcinoma [39], bladder cancer [40], gastric cancer [41], and hepatocellular carcinoma cells [42]. However, in our present study, inhibition of miR-195 itself significantly decreased the cell number, suggesting that the function of this miRNA might depend on the type of cancer cells.…”

Section: Discussioncontrasting

confidence: 52%

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

Ujifuku¹,

Mitsutake²,

Takakura³

et al. 2010

Cancer Letters

209

137

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Running title: miRNAs and temozolomide resistance in glioblastoma Key words: glioblastoma, resistance, microRNA,, miR-10a*, temozolomide. ABSTRACTTo identify microRNAs (miRNAs) specifically involved in the acquisition of temozolomide (TMZ) resistance in glioblastoma multiforme (GBM), we first established a resistant variant, U251R cells from TMZ-sensitive GBM cell line, U251MG. We then performed a comprehensive analysis of miRNA expressions in U251R and parental cells using miRNA microarrays. miR-195, miR-455-3p and miR-10a* were the three most up-regulated miRNAs in the resistant cells. To investigate the functional role of these miRNAs in TMZ resistance, U251R cells were transfected with miRNA inhibitors consisting of DNA/LNA hybrid oligonucleotides. Suppression of miR-455-3p or miR-10a* had no effect on cell growth, but showed modest cell killing effect in the presence of TMZ. On the other hand, knockdown of miR-195 alone displayed moderate cell killing effect, and combination with TMZ strongly enhanced the effect. In addition, using in silico analysis combined with cDNA microarray experiment, we present possible mRNA targets of these miRNAs. In conclusion, our findings suggest that those miRNAs may play a role in acquired TMZ resistance and could be a novel target for recurrent GBM treatment.

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Section: Discussioncontrasting

confidence: 52%

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

Ujifuku¹,

Mitsutake²,

Takakura³

et al. 2010

Cancer Letters

209

137

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“…Introduction of miR-195 markedly suppressed colony formation in vitro and tumor development in nude mice (24). MiR-497 expression was found to be downregulated in different cancers, such as primary peritoneal carcinoma, gastric cancer and breast cancer (23,27). However, the role of miR-497 in human cancer is not clear yet.…”

Section: Discussionmentioning

confidence: 99%

Analysis of MiR-195 and MiR-497 Expression, Regulation and Role in Breast Cancer

Zhao

Liu

et al. 2011

Clinical Cancer Research

286

257

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Purpose: To investigate expression, regulation, potential role and targets of miR-195 and miR-497 in breast cancer.Experimental Design: The expression patterns of miR-195 and miR-497 were initially examined in breast cancer tissues and cell lines by Northern blotting and quantitative real-time PCR. Combined bisulfite restriction analysis and bisulfite sequencing were carried out to study the DNA methylation status of miR-195 and miR-497 genes. Breast cancer cells stably expressing miR-195 and miR-497 were established to study their role and targets. Finally, normal, fibroadenoma and breast cancer tissues were employed to analyze the correlation between miR-195/497 levels and malignant stages of breast tumor tissues.Results: MiR-195 and miR-497 were significantly downregulated in breast cancer. The methylation state of CpG islands upstream of the miR-195/497 gene was found to be responsible for the downregulation of both miRNAs. Forced expression of miR-195 or miR-497 suppressed breast cancer cell proliferation and invasion. Raf-1 and Ccnd1 were identified as novel direct targets of miR-195 and miR-497. miR-195/497 expression levels in clinical specimens were found to be correlated inversely with malignancy of breast cancer.Conclusions: Our data imply that both miR-195 and miR-497 play important inhibitory roles in breast cancer malignancy and may be the potential therapeutic and diagnostic targets.

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“…Although, the down-regulation of miR-497 in a primary peritoneal carcinoma was shown [45], nothing is known about the importance of miR-497 in autoimmune disease or immune cells. Target prediction, based on sequence, suggests cadherin, T-cell activation and Wnt-pathway genes as possible targets, but none of them has been experimentally validated.…”

Section: T Cells and B Cells But Down-regulated In Cd8mentioning

confidence: 99%

Altered expression of miR‐17‐5p in CD4⁺ lymphocytes of relapsing–remitting multiple sclerosis patients

et al. 2010

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MicroRNA (miRNA) are a class of post-transcriptional regulators of gene expression targeting mRNA for translational repression and/or degradation. We analyzed the expression of 365 miRNA in lymphocytes in relapsing-remitting MS patients, and show the first evidence for distinct miRNA expression profiles in CD4 1 , CD81 and B cells in MS when compared with those in healthy volunteers. MiR-17-5p, which is involved in autoimmunity, was up-regulated in CD4 1 cells from MS patients. This was correlated with alterations in the expression of potential target genes of miR-17-5p, i.e. phosphatase and tensin homology and phosphatidyl-inositol-3-kinase regulatory subunit 1, which were down-regulated upon stimulation of CD4 1 cells with anti-CD3/CD28 in vitro. Functional experiments with a synthetic inhibitor of miR-17 supported the link between miRNA expression and the altered target gene expression. Moreover, we found distinct responses of deregulated miRNA to stimulation, i.e. miR-17-5p and miR-193a were strongly upregulated, in contrast to the down-regulation of miR-497, miR-1 and miR-126. Other deregulated miRNA did not respond to the stimulation probably due to other, non-T-cell activation related, mechanisms in their mode of action. Our findings support the role of miRNA-dependent regulatory mechanisms in the immunopathogenesis of MS.Key words: Autoimmune disease . Expression . Lymphocytes . MicroRNA . MS Supporting Information available onlineIntroduction MS results from a combination of environmental and genetic factors [1]. Genetic evidence suggests the existence of multiple susceptibility factors underlying MS. In the last couple of years, genomewide association studies have started to provide more information on genes that contribute to the risk of developing MS [2][3][4]. Large-scale transcriptional analysis with microarray technology has provided further insights into the molecular mechanisms of pathogenesis of MS. This approach has yielded several candidate genes responsible for the heterogeneous expression of the disease [5]. However, gene regulation is influenced by post-genomic regulatory mechanisms, e.g. micro-RNA (miRNA). MiRNA are small, endogenous non-coding RNA of approximately 22 nucleotides. They are transcribed in the nucleus, and after processing and export into the cytoplasm, they silence expression of target genes in a sequence-specific manner [6]. Repression of target genes is due to translational repression (imperfect sequence match) or mRNA cleavage (perfect match). MiRNA are key regulators of a wide variety of biological processes, e.g. cell proliferation and differentiation, apoptosis, signal transduction and organ development [7][8][9] It has been shown that miRNA are important in the homeostasis and function of the immune system [14][15][16][17]. Zhou et al. [18] showed that miR-150 is up-regulated during B-and T-cell maturation. Furthermore, Wu [19] reported different expression profiles of miRNA in antigen-specific naive, effector and memory CD8 1 T cells. In two recent reports [20,21...

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Potentially important microRNA cluster on chromosome 17p13.1 in primary peritoneal carcinoma

Cited by 79 publications

References 83 publications

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

Analysis of MiR-195 and MiR-497 Expression, Regulation and Role in Breast Cancer

Altered expression of miR‐17‐5p in CD4⁺ lymphocytes of relapsing–remitting multiple sclerosis patients

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Potentially important microRNA cluster on chromosome 17p13.1 in primary peritoneal carcinoma

Cited by 79 publications

References 83 publications

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

Analysis of MiR-195 and MiR-497 Expression, Regulation and Role in Breast Cancer

Altered expression of miR‐17‐5p in CD4+ lymphocytes of relapsing–remitting multiple sclerosis patients

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Altered expression of miR‐17‐5p in CD4⁺ lymphocytes of relapsing–remitting multiple sclerosis patients