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全球基因表达谱数据分析揭示了丝裂霉素在肉瘤细胞系中抑制的关键基因家族和生物学过程。

Global gene expression profiling data analysis reveals key gene families and biological processes inhibited by Mithramycin in sarcoma cell lines.

作者信息

Kulkarni Kirti K, Bankar Kiran Gopinath, Shukla Rohit Nandan, Das Chandrima, Banerjee Amrita, Dasgupta Dipak, Vasudevan Madavan

机构信息

Genome Informatics Research Group, Bionivid Technology Pvt Ltd., Bangalore 560043, India.

Biophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata 700064, India.

出版信息

Genom Data. 2014 Nov 8;3:8-14. doi: 10.1016/j.gdata.2014.11.001. eCollection 2015 Mar.

DOI:10.1016/j.gdata.2014.11.001
PMID:26484141
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4535529/
Abstract

The role of Mithramycin as an anticancer drug has been well studied. Sarcoma is a type of cancer arising from cells of mesenchymal origin. Though incidence of sarcoma is not of significant percentage, it becomes vital to understand the role of Mithramycin in controlling tumor progression of sarcoma. In this article, we have analyzed the global gene expression profile changes induced by Mithramycin in two different sarcoma lines from whole genome gene expression profiling microarray data. We have found that the primary mode of action of Mithramycin is by global repression of key cellular processes and gene families like phosphoproteins, kinases, alternative splicing, regulation of transcription, DNA binding, regulation of histone acetylation, negative regulation of gene expression, chromosome organization or chromatin assembly and cytoskeleton.

摘要

光辉霉素作为一种抗癌药物的作用已得到充分研究。肉瘤是一种起源于间充质细胞的癌症。尽管肉瘤的发病率占比不高,但了解光辉霉素在控制肉瘤肿瘤进展中的作用至关重要。在本文中,我们根据全基因组基因表达谱微阵列数据,分析了光辉霉素在两种不同肉瘤细胞系中诱导的全球基因表达谱变化。我们发现,光辉霉素的主要作用方式是全面抑制关键细胞过程和基因家族,如磷蛋白、激酶、可变剪接、转录调控、DNA结合、组蛋白乙酰化调控、基因表达的负调控、染色体组织或染色质组装以及细胞骨架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/7f7eee783401/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/a56d477948be/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/7414776c0165/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/eafc0a612271/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/45f0ba62e6ff/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/4b56468cc006/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/96196ead6db3/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/52c91bf69e80/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/7f7eee783401/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/a56d477948be/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/7414776c0165/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/eafc0a612271/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/45f0ba62e6ff/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/4b56468cc006/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/96196ead6db3/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/52c91bf69e80/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04f7/4535529/7f7eee783401/gr8.jpg

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