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Biochem Biophys Res Commun. 2014 Apr 18;446(4):1053-9. doi: 10.1016/j.bbrc.2014.03.064. Epub 2014 Mar 21.

USF-1 inhibition protects against oxygen-and-glucose-deprivation-induced apoptosis via the downregulation of miR-132 in HepG2 cells.

Author information

1
Department of Clinical Laboratory, Pingjin Hospital, Logistics College of Armed Police Forces, Tianjin, China.
2
Department of Neurosurgery, Pingjin Hospital, Logistics College of Armed Police Forces, Tianjin, China.
3
Department of Thoracic Surgery, Shandong Cancer Hospital and Institute, Jinan, Shandong, China.
4
Department of Clinical Laboratory, Pingjin Hospital, Logistics College of Armed Police Forces, Tianjin, China. Electronic address: wrm20142233@sohu.com.

Abstract

Upstream stimulatory factor 1 (USF-1) is an important transcription factor that participates in glucose metabolism and tumorigenesis. The aim of the current study was to explore the regulatory mechanism of USF-1 in HepG2 cells exposed to oxygen and glucose deprivation (OGD). After the establishment of the OGD model in HepG2 cells, we determined that the cells treated with OGD exhibited a high apoptotic rate and that the introduction of siRNA against USF-1 protected the cells from OGD-induced apoptosis. The miRNA microarray results demonstrated that a set of miRNAs were deregulated in the cells transfected with USF-1 siRNA, and the set of downregulated miRNAs included a novel miRNA, miR-132. Further analyses indicated that miR-132 overexpression inhibits the protective roles of USF-1 siRNA in OGD-induced apoptosis. We also identified several binding sites for USF-1 in the miR-132 promoter. The silencing of USF-1 resulted in a reduction in miR-132 expression, and USF-1 overexpression increased the expression of this miRNA. Our study indicated that the silencing of USF-1 plays protective roles in OGD-induced apoptosis through the downregulation of miR-132, which indicates that the silencing of USF-1 may be a therapeutic strategy for the promotion of cancer cell survival under OGD conditions.

KEYWORDS:

Apoptosis; Hepg2 cells; Oxygen and glucose deprivation; Upstream stimulatory factor 1; miR-132

PMID:
24661879
DOI:
10.1016/j.bbrc.2014.03.064
[Indexed for MEDLINE]

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