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DJ-1 upregulates breast cancer cell invasion by repressing KLF17 expression
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DJ-1 upregulates breast cancer cell invasion by repressing KLF17 expression
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Journal Article
DJ-1 upregulates breast cancer cell invasion by repressing KLF17 expression
2014
Overview
Background:
DJ-1 (PARK7) was reported as an oncogene in a Ras-dependent manner. Recent studies have shown that DJ-1 stimulates cell proliferation, cell invasion, and cancer metastasis. However, the molecular mehchanism by which DJ-1 induces cancer cell invasion and metastasis remains unclear.
Methods:
Breast cancer cells were transfected with DJ-1 siRNA or DJ-1 overexpression to investigate the effect of DJ-1 on KLF17 expression. ID-1 luciferase promoter assay was performed to evaluate DJ-1-dependent KLF17 expression changes. In addition, Epistasis analysis of DJ-1 and KLF17 was performed to evaluate their regulatory interactions. Ras inhibitors were pretreated to determine whether DJ-1 regulates cell invasion in a Ras-dependent manner.
Results:
In the present study, we found increased DJ-1 expression in highly invasive breast cancer cells as compared with non-metastatic cells. Furthermore, DJ-1 promoted breast cancer cell invasion by downregulating E-cadherin and increasing Snail expression. Interestingly, exogenous DJ-1 overexpression markedly decreased mRNA and protein expression of KLF17, the EMT negative regulator. These data were confirmed by ID-1 promoter activity, which is directly regulated by DJ-1-dependent KLF17 transcription factor. Epistasis analysis showed that KLF17 overexpression overcomes increased cell invasion by DJ-1, suggesting that KLF17 might be one of the downstream signalling molecules of DJ-1. Acceleration of cell invasion by DJ-1 was alleviated by Ras inhibitors, suggesting that DJ-1 cooperates with Ras to increase cell invasion.
Conclusion:
Altogether, these data suggest for the first time that DJ-1 acts as an EMT-positive regulator in breast cancer cells via regulation of the KLF17/ID-1 pathway.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Biological and medical sciences
/ Biomedical and Life Sciences
/ Breast Neoplasms - metabolism
/ Breast Neoplasms - pathology
/ Female
/ Gynecology. Andrology. Obstetrics
/ Humans
/ Intracellular Signaling Peptides and Proteins - genetics
/ Intracellular Signaling Peptides and Proteins - metabolism
/ Multiple tumors. Solid tumors. Tumors in childhood (general aspects)
/ Oncogene Proteins - genetics
/ Oncogene Proteins - metabolism
/ Oncology
/ Transcription Factors - antagonists & inhibitors
/ Transcription Factors - biosynthesis
/ Transcription Factors - genetics
/ Tumors
