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MiR-16 inhibits pituitary adenoma cell proliferation via the suppression of ERK/MAPK signal pathway.

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.

journal_name

Eur Rev Med Pharmacol Sci

journal_title

European review for medical and pharmacological sciences

authors

Wang DW,Wang YQ,Shu HS

doi

10.26355/eurrev_201803_14464

subject

Has Abstract

pub_date

2018-03-01 00:00:00

pages

1241-1248

issue

eissn

1128-3602

issn

2284-0729

journal_volume

pub_type

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MiR-16 inhibits pituitary adenoma cell proliferation via the suppression of ERK/MAPK signal pathway.