Dynamic changes in the expression of MicroRNA-31 during inflammatory bowel disease-associated neoplastic transformation.
Dynamic changes in the expression of MicroRNA-31 during inflammatory bowel disease-associated neoplastic transformation.
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DOI:
10.1002/ibd.21359
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发表时间:
2011-01
影响因子:
4.9
通讯作者:
Meltzer, Stephen J.
中科院分区:
文献类型:
--
作者:
Olaru, Alexandru V.;Selaru, Florin M.;Mori, Yuriko;Vazquez, Christine;David, Stefan;Paun, Bogdan;Cheng, Yulan;Jin, Zhe;Yang, Jian;Agarwal, Rachana;Abraham, John M.;Dassopoulos, Themistocles;Harris, Mary;Bayless, Theodore M.;Kwon, John;Harpaz, Noam;Livak, Ferenc;Meltzer, Stephen J.
关键词:
Patients with inflammatory bowel disease (IBD) are at increased risk of developing colorectal cancer. Aberrant microRNA (miRs) expression has been linked to carcinogenesis, however no reports document a relationship between IBD-related neoplasia (IBDN) and altered miR expression. In the current study we sought to identify specific miR dysregulation along the normal-inflammation-cancer axis. miR microarrays and quantitative RT-PCR were used to detect dysregulated miRs. Receiver operating characteristic curve analysis was employed to test for potential usefulness of miR-31 as a disease marker of IBDNs. In silico prediction analysis, Western blot, and luciferase activity measurement were employed for target identification. Several dysregulated miRs were identified between chronically inflamed mucosae and dysplasia arising in IBD. MiR-31 expression increases in a stepwise fashion during progression from normal to IBD to IBDN and accurately discriminated IBDNs from normal or chronically inflamed tissues in IBD patients. Finally, we identified factor inhibiting hypoxia inducible factor 1 as a direct target of miR-31. Our study reveals specific miR dysregulation as chronic inflammation progresses to dysplasia. MiR-31 expression levels increase with disease progression and accurately discriminates between distinct pathological entities that co-exist in IBD patients. The novel effect of miR-31 on regulating factor inhibiting hypoxia inducible factor 1 expression provides a new insight on the pathogenesis of IBDN.
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影响因子:
11.2
作者:
Liu, Chung-Ji;Tsai, Meng-Miao;Chang, Kuo-Wei
通讯作者:
Chang, Kuo-Wei
DOI:
10.1073/pnas.0602266103
发表时间:
2006-05-02
影响因子:
11.1
作者:
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通讯作者:
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影响因子:
29.4
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7.3
作者:
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通讯作者:
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