The regulatory mechanism of ATRA- and Am80-induced HL-60 cell differentiation: miRNA and gene network

碩士 === 國立臺灣大學 === 分子與細胞生物學研究所 === 95 === All-trans retinoic acid (ATRA) and Am80, natural and synthetic derivatives of Vitamin A, have been used in oncology for many years and are useful for inducing HL-60 to differentiate to granulocyte. In this study, we showed that TGF-β signaling pathway is the...

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Main Authors: Cheng-Pao Chen, 陳正寶
Other Authors: 阮雪芬
Format: Others
Language:zh-TW
Published: 2007
Online Access:http://ndltd.ncl.edu.tw/handle/41677283331783507351
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spelling ndltd-TW-095NTU050610182015-12-07T04:04:29Z http://ndltd.ncl.edu.tw/handle/41677283331783507351 The regulatory mechanism of ATRA- and Am80-induced HL-60 cell differentiation: miRNA and gene network ATRA與Am80誘導HL-60分化的調控機制:微型核醣核酸與基因網路 Cheng-Pao Chen 陳正寶 碩士 國立臺灣大學 分子與細胞生物學研究所 95 All-trans retinoic acid (ATRA) and Am80, natural and synthetic derivatives of Vitamin A, have been used in oncology for many years and are useful for inducing HL-60 to differentiate to granulocyte. In this study, we showed that TGF-β signaling pathway is the most perturbed and involved in differentiation process using microarray and bioinformatics approach. With time-series gene expression profiles measured by the quantitative real-time PCR, we constructed a gene network of ATRA- and Am80-induced human leukemia cell line HL-60 differentiation. The results from comparative analysis of target genes indicated that this gene network was regulated by some candidate microRNAs. MicroRNAs are non-coding, single-stranded RNAs of 20 ~ 25 nucloetides that execute a gene regulator function responsible for cell growth, cell differentiation, disease, and cancer. In our results, the expression of miR-96 and miR-107 were significantly induced by ATRA and Am80. In summary, our results showed that miR-96 and miR-107 seem to be the regulators involved in the gene network of leukemia cell differentiation. 阮雪芬 2007 學位論文 ; thesis 155 zh-TW
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description 碩士 === 國立臺灣大學 === 分子與細胞生物學研究所 === 95 === All-trans retinoic acid (ATRA) and Am80, natural and synthetic derivatives of Vitamin A, have been used in oncology for many years and are useful for inducing HL-60 to differentiate to granulocyte. In this study, we showed that TGF-β signaling pathway is the most perturbed and involved in differentiation process using microarray and bioinformatics approach. With time-series gene expression profiles measured by the quantitative real-time PCR, we constructed a gene network of ATRA- and Am80-induced human leukemia cell line HL-60 differentiation. The results from comparative analysis of target genes indicated that this gene network was regulated by some candidate microRNAs. MicroRNAs are non-coding, single-stranded RNAs of 20 ~ 25 nucloetides that execute a gene regulator function responsible for cell growth, cell differentiation, disease, and cancer. In our results, the expression of miR-96 and miR-107 were significantly induced by ATRA and Am80. In summary, our results showed that miR-96 and miR-107 seem to be the regulators involved in the gene network of leukemia cell differentiation.
author2 阮雪芬
author_facet 阮雪芬
Cheng-Pao Chen
陳正寶
author Cheng-Pao Chen
陳正寶
spellingShingle Cheng-Pao Chen
陳正寶
The regulatory mechanism of ATRA- and Am80-induced HL-60 cell differentiation: miRNA and gene network
author_sort Cheng-Pao Chen
title The regulatory mechanism of ATRA- and Am80-induced HL-60 cell differentiation: miRNA and gene network
title_short The regulatory mechanism of ATRA- and Am80-induced HL-60 cell differentiation: miRNA and gene network
title_full The regulatory mechanism of ATRA- and Am80-induced HL-60 cell differentiation: miRNA and gene network
title_fullStr The regulatory mechanism of ATRA- and Am80-induced HL-60 cell differentiation: miRNA and gene network
title_full_unstemmed The regulatory mechanism of ATRA- and Am80-induced HL-60 cell differentiation: miRNA and gene network
title_sort regulatory mechanism of atra- and am80-induced hl-60 cell differentiation: mirna and gene network
publishDate 2007
url http://ndltd.ncl.edu.tw/handle/41677283331783507351
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