@Article{096504019X15761465603129,
AUTHOR = {Daniela D’Angelo, Claudio Arra, Alfredo Fusco},
TITLE = {RPSAP52 lncRNA Inhibits p21Waf1/CIP Expression by Interacting With  the RNA Binding Protein HuR},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {2},
PAGES = {191--201},
URL = {http://www.techscience.com/or/v28n2/48543},
ISSN = {1555-3906},
ABSTRACT = {Long noncoding RNAs have been recently demonstrated to have an important role in fundamental biological processes, and their deregulated expression has been found in several human neoplasias. Our group has 
recently reported a drastic overexpression of the long noncoding RNA (lncRNA) RPSAP52 (ribosomal protein SA pseudogene 52) in pituitary adenomas. We have shown that this lncRNA increased cell proliferation 
by upregulating the expression of the chromatinic proteins HMGA1 and HMGA2, functioning as a competing endogenous RNA (ceRNA) through competitively binding to microRNA-15a (miR-15a), miR-15b, and 
miR-16. The aim of this work was to identify further mechanisms by which RPSAP52 overexpression could 
contribute to the development of pituitary adenomas. We investigated the involvement of RPSAP52 in the 
modulation of the expression of cell cycle-related genes, such as p21Waf1/CIP, whose deregulation plays a 
critical role in pituitary cell transformation. We report that RPSAP52, interacting with the RNA binding protein 
HuR (human antigen R), favors the delocalization of miR-15a, miR-15b, and miR-16 on the cyclin-dependent 
kinase inhibitor p21Waf1/CIP1 that, accordingly, results in downregulation in pituitary adenomas. A RNA 
immunoprecipitation sequencing (RIPseq) analysis performed on cells overexpressing RPSAP52 identified 40 
messenger RNAs (mRNAs) enriched in Argonaute 2 (AGO2) immunoprecipitated samples. Among them, we 
focused on GAS8 (growth arrest-specific protein 8) gene. Consistently, GAS8 expression was downregulated 
in all the analyzed pituitary adenomas with respect to normal pituitary and in RPSAP52-overepressing cells, 
supporting the role of RPSAP52 in addressing genes involved in growth inhibition and cell cycle arrest to 
miRNA-induced degradation. This study unveils another RPSAP52-mediated molecular mechanism in pituitary tumorigenesis.},
DOI = {10.3727/096504019X15761465603129}
}