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@ARTICLE{Laudato:128080,
author = {S. Laudato$^*$ and N. S. Patil$^*$ and M. L. Abba$^*$ and
J. H. Leupold$^*$ and A. Benner$^*$ and T. Gaiser and A.
Marx and H. Allgayer$^*$},
title = {{P}53-induced mi{R}-30e-5p inhibits colorectal cancer
invasion and metastasis by targeting {ITGA}6 and {ITGB}1.},
journal = {International journal of cancer},
volume = {141},
number = {9},
issn = {0020-7136},
address = {Bognor Regis},
publisher = {Wiley-Liss},
reportid = {DKFZ-2017-04102},
pages = {1879 - 1890},
year = {2017},
abstract = {The tumor suppressor P53 is a critical regulator of normal
cellular homeostasis whose function is either distorted or
lost in several cancer types including colorectal cancer
(CRC). A small group of microRNAs have come to be recognized
as essential mediators of P53 function. In a genome-wide
systematic approach, we explored miRNAs that are
substantially altered by P53 loss and found miR-30e to be
the most significantly deregulated miRNA in P53-knockout
human CRC cells. We identified miR-30e-5p to be a novel
direct transcriptional target of P53 with gain and loss of
function experiments revealing miR-30e-5p to be a
significant regulator of tumor cell migration, invasion and
in vivo metastasis mediated in part by integrins alpha-6 and
beta-1 as novel targets. MiR-30e-5p also significantly
reduced tumor cell proliferation by causing G1/S cell cycle
arrest, which was achieved by inducing P21 and P27
expression. Finally, we found miR-30e-5p to be lost in
resected CRC tumors as compared to normal colon tissues.
Taken together, miR-30e-5p is a novel effector of
P53-induced suppression of migration, invasion and
metastasis.},
cin = {G360 / C060},
ddc = {610},
cid = {I:(DE-He78)G360-20160331 / I:(DE-He78)C060-20160331},
pnm = {317 - Translational cancer research (POF3-317)},
pid = {G:(DE-HGF)POF3-317},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28656629},
doi = {10.1002/ijc.30854},
url = {https://inrepo02.dkfz.de/record/128080},
}