1,724,729 research outputs found
miR-6734 targets p21 promoter and induces p21 gene expression.
No full text(A) Sequence of dsP21-322 and miR-6734 target site located at nucleotide -322 relative to the transcriptional start site in p21 promoter. (B) Five human cancer cells were transfected with miR-6734 at 10nmol/L for 72h. The mRNA expression of p21 was analyzed by qPCR. (C) HCT-116 cells were transfected with mock and miR-6734-5P inhibitor at 30 nmol/L for 72 h. The mRNA expression of p21 was analyzed by qPCR. Data are presented as mean ± S.D. of quadruplicate experiments. Statistical significance was analyzed by one-way ANOVA and Dunnett’s t-test (* p < 0.05; ** p < 0.01 versus mock). (D) HCT-116 cells were transfected with biotin-labeled miR-6734 and chromatin immunoprecipitation (ChIP) assays were performed by using antibodies against biotin to pull down associated DNA. The precipitated DNA was amplified by PCR using primer sets specific to miR-6734 target sites (-360/-260) of p21 promoter. Input DNA was amplified as a loading control. DNA pulled down by the anti-IgG antibody was served to identify background amplification. Duplicate samples were analyzed for each treatment.</p
miR-6734 Up-Regulates p21 Gene Expression and Induces Cell Cycle Arrest and Apoptosis in Colon Cancer Cells.
No full textRecently, microRNAs have been implicated in the regulation of gene expression in terms of both gene silencing and gene activation. Here, we investigated the effects of miR-6734, which has a sequence homology with a specific region of p21WAF1/CIP1 (p21) promoter, on cancer cell growth and the mechanisms involved in this effect. miR-6734 up-regulated p21 expression at both mRNA and protein levels and chromatin immunoprecipitation analysis using biotin-labeled miR-6734 confirmed the association of miR-6734 with p21 promoter. Moreover, miR-6734 inhibited cancer cell growth and induced cell cycle arrest and apoptosis in HCT-116 cells, which was abolished by knockdown of p21. The phosphorylation of Rb and the cleavage of caspase 3 and PARP were suppressed by miR-6734 transfection in HCT-116 cells and these effects were also reversed by p21 knockdown. In addition, miR-6734 transfection caused prolonged induction of p21 gene and modification of histones in p21 promoter, which are typical aspects of a phenomenon referred to as RNA activation (RNAa). Collectively, our results demonstrated that miR-6734 inhibits the growth of colon cancer cells by up-regulating p21 gene expression and subsequent induction of cell cycle arrest and apoptosis, suggesting its role as an important endogenous regulator of cancer cell proliferation and survival
Abstract 1464: miR-6734 induces cell cycle arrest and apoptosis via up-regulation of p21 expression in colon cancer cells
No full textAbstract
Recently, microRNAs have been implicated in the regulation of gene expression in terms of both gene silencing and gene activation. Here, we investigated the effects of miR-6734, which has a sequence homology with a specific region of p21WAF1/CIP1 (p21) promoter, on cancer cell growth and the mechanisms involved in this effect. miR-6734 up-regulated p21 expression at both mRNA and protein levels and chromatin immunoprecipitation analysis using biotin-labeled miR-6734 confirmed the association of miR-6734 with p21 promoter. Moreover, miR-6734 inhibited cancer cell growth and induced cell cycle arrest and apoptosis in HCT-116 cells, which was abolished by knockdown of p21. The phosphorylation of Rb and the cleavage of caspase 3 and PARP were suppressed by miR-6734 transfection in HCT-116 cells and these effects were also reversed by p21 knockdown. In addition, miR-6734 transfection caused prolonged induction of p21 gene and modification of histones in p21 promoter, which are typical aspects of a phenomenon referred to as RNA activation (RNAa). Collectively, our results demonstrated that miR-6734 inhibits the growth of colon cancer cells by up-regulating p21 gene expression and subsequent induction of cell cycle arrest and apoptosis, suggesting its role as an important endogenous regulator of cancer cell proliferation and survival.
Citation Format: Jong Soon Kang, Moo Rim Kang. miR-6734 induces cell cycle arrest and apoptosis via up-regulation of p21 expression in colon cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1464. doi:10.1158/1538-7445.AM2017-1464</jats:p
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Histone modification of p21 promoter by miR-6734.
No full textChromatin immunoprecipitation (ChIP) assays were performed by using antibodies against IgG, di-methyl-histone-H3-lysine 9 (H3K9me2), acetyl-histone-H2B (H2Bac) and acetyl-histone-H3 (H3ac) to pull down associated DNA. The precipitated DNA was amplified by RT-PCR using primer sets specific to miR-6734 target sites (-360/-260) of p21 gene promoter. Input DNA was amplified as a loading control. DNA pulled down in the IgG antibody served to identify background amplification.</p
Variations on the Author
Get PDF“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
miR-6734 induces apoptosis in HCT-116 cells.
No full textHCT-116 cells were treated with mock, dsCon or the indicated concentrations of miR-6734 for 72 h. (A) Transfected cells were stained with propidium iodide and annexin V-FITC and apoptotic cells were measured by flow cytometry. (B) The percentage of early and late apoptotic cells were calculated using the WinMDI program. (C) Culture supernatants were collected, and the activity of caspase-3/7 was determined via caspase-Glo 3/7 assay kit. Data are presented as mean ± S.D. of triplicate experiments. Statistical significance was analyzed by one-way ANOVA and Dunnett’s t-test (** p < 0.01; *** p < 0.001 versus mock).</p
Appropriate Similarity Measures for Author Cocitation Analysis
Get PDFWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
miR-6734 induces cell cycle arrest in HCT-116 cells.
No full textHCT-116 cells were transfected with mock, dsCon or the indicated concentrations of miR-6734 for 48 h. (A) Cell cycle distribution was examined by flow cytometry. (B) The percentage of cells in G0/G1, S, and G2/M phases were calculated using the ModFit program. Data are presented as mean ± S.D. of triplicate experiments. Statistical significance was analyzed by one-way ANOVA and Dunnett’s t-test (** p < 0.01; *** p < 0.001 versus mock). (C) Protein levels of p21, cyclin-A, p-Rb and GAPDH in the total cell lysates were determined by Western Immunoblot analysis.</p
- …
