F
Fangting Wu
Researcher at Southern Illinois University School of Medicine
Publications - 13
Citations - 4581
Fangting Wu is an academic researcher from Southern Illinois University School of Medicine. The author has contributed to research in topics: microRNA & Gene silencing. The author has an hindex of 12, co-authored 12 publications receiving 4303 citations. Previous affiliations of Fangting Wu include Southern Illinois University Carbondale.
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Journal ArticleDOI
miR-21-mediated tumor growth
TL;DR: The results suggest that miR-21 functions as an oncogene and modulates tumorigenesis through regulation of genes such as bcl-2 and thus, it may serve as a novel therapeutic target.
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MicroRNA-21 targets tumor suppressor genes in invasion and metastasis
TL;DR: In this article, the role of mir-21 in cell invasion and tumor metastasis was investigated in metastatic breast cancer MDA-MB-231 cells, and it was shown that suppressing the expression of the tumor suppressor gene tropomyosin 1 (TPM1) significantly reduced cell invasion.
Journal ArticleDOI
p53 represses c-Myc through induction of the tumor suppressor miR-145
Mohit Sachdeva,Shoumin Zhu,Fangting Wu,Hailong Wu,Vijay Walia,Sumit Kumar,Randolph C. Elble,Kounosuke Watabe,Yin-Yuan Mo +8 more
TL;DR: The role of miR-145 is defined in the posttranscriptional regulation of c-Myc by p53 and it is suggested that, as a new member of the p53 regulatory network, mi R-145 provides a direct link between p 53 and c- myc in this gene regulatory network.
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LncRNA loc285194 is a p53-regulated tumor suppressor
Qian Liu,Jianguo Huang,Nanjiang Zhou,Ziqiang Zhang,Ali Zhang,Zhaohui Lu,Fangting Wu,Yin-Yuan Mo +7 more
TL;DR: It is suggested that loc285194 is a p53-regulated tumor suppressor, which acts in part through repression of miR-211, and downregulation of loc285 194 in colon cancer specimens is detected.
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Targeting non-coding RNAs with the CRISPR/Cas9 system in human cell lines
Tsui-Ting Ho,Nanjiang Zhou,Jianguo Huang,Pratirodh Koirala,Min Xu,Roland Fung,Fangting Wu,Yin-Yuan Mo +7 more
TL;DR: The results demonstrate the feasibility of knockout for non-coding genes by the CRISPR/Cas system in human cell lines and show that the HR-mediated targeting efficiency can be further improved by suppression of the non-homologous end joining pathway.