TC3A: The Cancer 3' UTR Atlas.

TC3A: The Cancer 3' UTR Atlas.
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DOI:
10.1093/nar/gkx892
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发表时间:
2018-01-04
影响因子:
14.9
通讯作者:
Li W
Li W
中科院分区:
生物学2区
文献类型:
--
作者:
Feng X;Li L;Wagner EJ;Li W

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在增强的细胞增殖和转化过程中,广泛的交替多聚腺苷酸化(APA)发生。最近,我们证明了CFIm25介导的3 ′ UTR缩短通过APA促进胶质母细胞瘤肿瘤生长在体外和体内,进一步强调其对肿瘤发生的意义。在这里,我们报告了癌症3 ′ UTR图谱(TC3A),这是一个关于APA在32种癌症类型中使用10,537种肿瘤的综合资源。这些APA事件代表了潜在的新型预后生物标志物,并可能揭示癌症驱动基因调控的新机制。TC3A建立在现在事实上的标准cBioPortal之上。因此,现有cBioPortal用户和临床研究人员的大型社区将发现TC3A熟悉并立即可用。TC3A目前功能齐全,可在www.example.com上免费获得。
Widespread alternative polyadenylation (APA) occurs during enhanced cellular proliferation and transformation. Recently, we demonstrated that CFIm25-mediated 3′ UTR shortening through APA promotes glioblastoma tumor growth in vitro and in vivo, further underscoring its significance to tumorigenesis. Here, we report The Cancer 3′ UTR Atlas (TC3A), a comprehensive resource of APA usage for 10,537 tumors across 32 cancer types. These APA events represent potentially novel prognostic biomarkers and may uncover novel mechanisms for the regulation of cancer driver genes. TC3A is built on top of the now de facto standard cBioPortal. Therefore, the large community of existing cBioPortal users and clinical researchers will find TC3A familiar and immediately usable. TC3A is currently fully functional and freely available at http://tc3a.org.
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