% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{AmayaRamirez:277770,
author = {C. C. Amaya Ramirez$^*$ and F. Loayza-Puch$^*$},
title = {{B}reast {C}ancer {M}etastatic {P}rogression {R}equires
m{RNA} {P}osttranscriptional {S}uppression.},
journal = {Cancer research},
volume = {83},
number = {15},
issn = {0099-7013},
address = {Philadelphia, Pa.},
publisher = {AACR},
reportid = {DKFZ-2023-01485},
pages = {2448-2449},
year = {2023},
note = {#EA:B250#LA:B250# / 2023 Aug 1;83(15):2448-2449 / IN THE
SPOTLIGHT},
abstract = {Cancer cell survival is highly dependent on its metabolic
reprogramming, which supports not only cell growth but also
confers to the tumor cells characteristics to initiate
migration and colonization. Among the different mechanisms
that are involved, translational control plays a significant
role in oncogenesis; however, its impact on cancer
progression still remains poorly understood. A study by
Navickas and colleagues revealed that the RNA-binding
protein heterogeneous nuclear ribonucleoprotein C (HNRNPC)
functions as a translational regulator, and its
downregulation in highly metastatic cells leads to the
lengthening of 3' untranslated regions in HNRNPC-bound
mRNAs, resulting in translational repression mediated by the
AGO-miRNA RNA-induced silencing complex.},
cin = {B250},
ddc = {610},
cid = {I:(DE-He78)B250-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37470809},
doi = {10.1158/0008-5472.CAN-23-1729},
url = {https://inrepo02.dkfz.de/record/277770},
}