The PI3K-Akt pathway is one of the most commonly dysregulated cancer-associated signaling pathways. Here we report an oncogenic function for the miR-181 family in luminal breast cancer cells that involves Akt hyperactivation. We show that miR-181a and miR-181d posttranscriptionally suppress the expression of PHLPP2 and INPP4B phosphatases, resulting in elevated growth factor-induced Akt phosphorylation. Ectopic expression of miR-181a and miR-181d promoted S-phase entry and cell proliferation, which was reversed by pharmacological Akt inhibition. Importantly, the expression of miR-181 family members and PHLPP2/INPP2B are inversely correlated in primary human estrogen receptor-positive breast cancers, supporting the clinical relevance of our findings.
%0 Journal Article
%1 Strotbek2017
%A Strotbek, Michaela
%A Schmid, Simone
%A Sánchez-González, Ismael
%A Boerries, Melanie
%A Busch, Hauke
%A Olayioye, Monilola A.
%D 2017
%J International Journal of Cancer
%K 2017 izi olayioye
%N 10
%P 2310--2320
%R 10.1002/ijc.30661
%T miR-181 elevates Akt signaling by co-targeting PHLPP2 and INPP4B phosphatases in luminal breast cancer
%U http://www.ncbi.nlm.nih.gov/pubmed/28224609
%V 140
%X The PI3K-Akt pathway is one of the most commonly dysregulated cancer-associated signaling pathways. Here we report an oncogenic function for the miR-181 family in luminal breast cancer cells that involves Akt hyperactivation. We show that miR-181a and miR-181d posttranscriptionally suppress the expression of PHLPP2 and INPP4B phosphatases, resulting in elevated growth factor-induced Akt phosphorylation. Ectopic expression of miR-181a and miR-181d promoted S-phase entry and cell proliferation, which was reversed by pharmacological Akt inhibition. Importantly, the expression of miR-181 family members and PHLPP2/INPP2B are inversely correlated in primary human estrogen receptor-positive breast cancers, supporting the clinical relevance of our findings.
%@ 4971168569301
@article{Strotbek2017,
abstract = {The PI3K-Akt pathway is one of the most commonly dysregulated cancer-associated signaling pathways. Here we report an oncogenic function for the miR-181 family in luminal breast cancer cells that involves Akt hyperactivation. We show that miR-181a and miR-181d posttranscriptionally suppress the expression of PHLPP2 and INPP4B phosphatases, resulting in elevated growth factor-induced Akt phosphorylation. Ectopic expression of miR-181a and miR-181d promoted S-phase entry and cell proliferation, which was reversed by pharmacological Akt inhibition. Importantly, the expression of miR-181 family members and PHLPP2/INPP2B are inversely correlated in primary human estrogen receptor-positive breast cancers, supporting the clinical relevance of our findings.},
added-at = {2018-02-01T14:15:48.000+0100},
author = {Strotbek, Michaela and Schmid, Simone and S{\'{a}}nchez-Gonz{\'{a}}lez, Ismael and Boerries, Melanie and Busch, Hauke and Olayioye, Monilola A.},
biburl = {https://puma.ub.uni-stuttgart.de/bibtex/23dfc438e479e9c545aadf206a7838e04/cristiano},
doi = {10.1002/ijc.30661},
interhash = {11211f5f43e81d19810cb01b8c0e9e06},
intrahash = {3dfc438e479e9c545aadf206a7838e04},
isbn = {4971168569301},
issn = {10970215},
journal = {International Journal of Cancer},
keywords = {2017 izi olayioye},
month = may,
number = 10,
pages = {2310--2320},
pmid = {28224609},
timestamp = {2019-01-17T12:28:55.000+0100},
title = {{miR-181 elevates Akt signaling by co-targeting PHLPP2 and INPP4B phosphatases in luminal breast cancer}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/28224609},
volume = 140,
year = 2017
}
