NDLI: MicroRNA-21 activation of Akt via PTEN is involved in the epithelial–mesenchymal transition and malignant transformation of human keratinocytes induced by arsenite

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MicroRNA-21 activation of Akt via PTEN is involved in the epithelial–mesenchymal transition and malignant transformation of human keratinocytes induced by arsenite

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Toxicology Research Vol - 5 Issue - 3

Toxicology Research Vol - 5 Issue - 2

Toxicology Research Vol - 5 Issue - 1

Toxicology Research Vol -4

Toxicology Research Vol -3

Toxicology Research Vol -2

Toxicology Research Vol -1

MicroRNA-21 activation of Akt via PTEN is involved in the epithelial–mesenchymal transition and malignant transformation of human keratinocytes induced by arsenite

Content Provider	Royal Society of Chemistry (RSC)
Author	Li, Jun Liu, Qizhan Lu, Lu Xue, Junchao Liu, Xinlu Luo, Fei Shi, Le Liu, Yang Fan, Weimin Xu, Hui Lu, Xiaolin Zhang, Aihua
Copyright Year	2016
Abstract	MicroRNAs are involved in the epithelial–mesenchymal transition (EMT) and malignant transformation of cells. However, the molecular mechanisms remain unclear. In seeking new biomarkers of chemical exposure in the risk assessment of arsenite-induced skin cancer, the function of microRNA-21 (miR-21) in the regulation of serine/threonine kinase (Akt) activation was investigated. Akt suppresses phosphatase and tensin homolog (PTEN) and is involved in neoplastic and metastatic properties of arsenite-transformed human keratinocyte (T-HaCaT) cells. In HaCaT cells, arsenite caused an increase of miR-21 levels and a decrease of PTEN, which activated Akt signaling and induced the EMT. On inhibiting miR-21, the levels of PTEN were increased, and activation of Akt was blocked. Knock-down of PTEN by siRNA enhanced the activation of Akt. The effects of an miR-21 inhibitor on Akt activation were antagonized by PTEN siRNA. In T-HaCaT cells, blocking the activation of Akt by LY294002 inhibited the EMT. Moreover, the effects of an miR-21 mimic on the EMT and the neoplastic capacity, invasion, and metastasis of T-HaCaT cells were antagonized by LY294002. T-HaCaT transfected with PTEN plasmids showed decreased Akt activation and E-cadherin expression and increased vimentin levels. Thus, activation of Akt, controlled by miR-21/PTEN, is involved in the EMT, and thereby affects the neoplastic, invasion, and migratory capacities of T-HaCaT cells. The results point to the potential use of miR-21 as a biomarker for skin cancer and as a target for cancer prevention and treatment.
Starting Page	1140
Ending Page	1147
Page Count	8
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	5
Issue Number	4
Journal	Toxicology Research
DOI	10.1039/c6tx00041j
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Vimentin Biomarker Protein kinase B LY294002 Threonine Serine MIRN21 PTEN Small interfering RNA Enzyme inhibitor Akt Metastasis Phosphatase Cadherin Epithelial\u2013mesenchymal transition Skin cancer Kinase Keratinocyte Prime Time Entertainment Network Arsenite HaCaT Cancer
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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