MicroRNA-132 targets PEA-15 and suppresses the progression of astrocytoma in vitro.

Abstract

Gliomas are highly malignant tumors, the most common of which are astrocytomas. A growing number of studies suggest that dysregulation of miRNAs is a frequent event contributing to the pathogenesis of gliomas. In this study, we found that over-expression of miR-132 inhibited cell proliferation and migration and triggered apoptosis, while knockdown of miR-132 showed opposite effects. PEA-15 was identified as a direct target of miR-132. Reintroduction of PEA-15 without 3'UTR region reversed the inhibitory effects of miR-132 on cell proliferation, migration, and apoptosis. MiR-132 was inversely correlated with the PEA-15 expression. CREB (cAMP response element binding protein) and KLF (Krüppel-like factor 8) were conformed as transcription factors of miR-132, which bidirectionally regulate the expression of miR-132. Our study suggests that miR-132 is an important tumor suppressor of astrocytoma progression by targeting PEA-15, while CREB and KLF can modulate the expression of miR-132, thus providing new insight into the molecular mechanisms underlying astrocytoma progression in vitro.

• Authors: Fei Geng, Jian-Lin Wu, Gui-Feng Lu, Zhi-Ping Liang, Zhuo-Li Duan, Xi Gu
• Journal: Journal of neuro-oncology (J Neurooncol) Vol. 129 Issue 2 Pg. 211-20 (09 2016) ISSN: 1573-7373 [Electronic] United States
• PMID: 27294355 (Publication Type: Journal Article)

Chemical References

• Apoptosis Regulatory Proteins
• Intracellular Signaling Peptides and Proteins
• KLF8 protein, human
• Kruppel-Like Transcription Factors
• MIRN132 microRNA, human
• MicroRNAs
• PEA15 protein, human
• Phosphoproteins
• RNA, Messenger
• Repressor Proteins
• CREB-Binding Protein
• Sincalide

Topics

• Analysis of Variance
• Apoptosis (genetics, physiology)
• Apoptosis Regulatory Proteins
• Astrocytoma (metabolism, pathology)
• Brain Neoplasms (metabolism, pathology)
• CREB-Binding Protein (genetics, metabolism)
• Cell Line, Tumor
• Cell Movement (genetics, physiology)
• Cell Proliferation (genetics, physiology)
• Disease Progression
• Gene Expression Regulation, Neoplastic (genetics, physiology)
• Glioma
• HEK293 Cells
• Humans
• Intracellular Signaling Peptides and Proteins (metabolism)
• Kruppel-Like Transcription Factors
• MicroRNAs (genetics, metabolism)
• Phosphoproteins (metabolism)
• RNA, Messenger
• Repressor Proteins (genetics, metabolism)
• Sincalide (metabolism)
• Time Factors
• Transfection