MiR-16 inhibits pituitary adenoma cell proliferation via the suppression of ERK/MAPK signal pathway
Authors: D-W Wang
Y-Q Wang
H-S Shu
Journal: European Review for Medical and Pharmacological Sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: ERK/MAPK pathway; miR-16; pituitary tumor; cell proliferation; apoptosis
Affiliations: Department of Neurosurgery, the Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, People's Republic of China. .

Abstract:  Objective: Extracellular signal-regulated kinase (ERK)/mitogen activated protein kinase (MAPK) signal pathway participates in cell proliferation, cycle, and apoptosis. MiR-16 is down-regulated in the pituitary tumor. This study investigated the role and related mechanism of miR-16 on pituitary tumor proliferation, cycle, and apoptosis. Patients and methods: Dual-luciferase reporter assay was conducted to demonstrate the targeted regulation between miR-16 and MEK1. MiiR-16, MEK1, p-ERK1/2, Survivin and Cyclin D1 expression were compared between normal embryonic pituitary cells, HP75 tumor cells. Flow cytometry detection measured cell proliferation and cycle. Cultured HP75 cells were divided into four groups: miR-NC, miR-16 mimic, si-NC, and si-MEK1. Expressions of miR-16, MEK1, p-ERK1/2, Survivin, and Cyclin D1 were compared, and cell proliferation, cycle, and apoptosis were tested by flow cytometry. Results: Bioinformatics analysis showed complementary binding sites between miR-16 and MEK1. Dual luciferase reporter assay validated the direct regulation between miR-16 and MEK1. Compared to that of normal pituitary tissues, significantly lower miR-16 expression, but higher MEK1 level were found in adenoma tissues. Compared to normal embryonic pituitary cells, the level of miR-16 was decreased, while the expressions of p-ERK1/2, Survivin, and Cyclin D1, along with cell proliferation or S or G2/M phase ratio were up-regulated in the group of HP75 cells. Transfection of miR-16 mimic or si-MEK1 remarkably suppressed the expressions of MEK1, p-ERK1/2, Survivin or Cyclin D1 in HP75 cells, inhibited cell proliferation and induced apoptosis and cycle arrest. Conclusions: MiR-16 inhibited ERK/MAPK pathway activity via the suppression of MEK1 expression, and further suppressed proliferation of pituitary tumor cells. 

Retracted: Yes

PubPeer comments:
   The Western Blots in this paper are sharp-edged black oval blobs on a featureless grey background. These are among the characteristics of [a papermill discussed here] , with examples listed in a Google document. https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit#gid=0 One of the common features of the papermill is a disconnection between the name of the putative corresponding author and the email address provided for correspondence.  , 
 Withdrawn. https: www.europeanreview.org article 22992 *Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, u201cMiR-16 inhibits pituitary adenoma cell proliferation via the suppression of ERK MAPK signal pathway, by D.-W. Wang, Y.-Q. Wang, H.-S. Shu, published in Eur Rev Med Pharmacol Sci 2018; 22 (5): 1241-1248u2013DOI: 10.26355 eurrev_201803_14464u2013PMID: 29565480u201d has been withdrawn.* *The Publisher apologizes for any inconvenience this may cause.* ,