Nuclear transcription factor Nrf2 suppresses prostate cancer cells growth and migration through upregulating ferroportin

Dong Xue; Cuixing Zhou; Yunbo Shi; Hao Lu; Renfang Xu; Xiaozhou He

doi:10.18632/oncotarget.12860

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

Research Papers:

Nuclear transcription factor Nrf2 suppresses prostate cancer cells growth and migration through upregulating ferroportin

Dong Xue, Cuixing Zhou, Yunbo Shi, Hao Lu, Renfang Xu and Xiaozhou He _

PDF | HTML | How to cite

Oncotarget. 2016; 7:78804-78812. https://doi.org/10.18632/oncotarget.12860

Metrics: PDF 3324 views | HTML 4865 views | ?

Abstract

Dong Xue1, Cuixing Zhou1, Yunbo Shi 2, Hao Lu1, Renfang Xu1, Xiaozhou He1

1Department of Urology, Third Affiliated Hospital, Suzhou University, Changzhou 213003, Jiangsu, China

2Foreign Languages School, Changzhou Institute of Technology, Changzhou 213002, Jiangsu, China

Correspondence to:

Xiaozhou He, email: [email protected]

Keywords: prostate cancer, ferroportin, Nrf2, ferritin, apoptosis

Received: July 29, 2016 Accepted: October 04, 2016 Published: October 24, 2016

ABSTRACT

VTo investigate the effect of nuclear transcription factor Nrf2 on the transcription of Ferroportin (FPN) in prostate cancer cells, and the regulation mechanisms of FPN on cell viability, migration and apoptosis of prostate cancer cells.

Empty vectors, pEGFPC1-Nrf2, pEGFPC1-FPN, Si-FPN and Si-Nrf2 were transfected into prostate cancer cell line PC3. The expression of mRNA and protein were measured by real time-PCR (RT-PCR) and western blot. Cell viability, migration, cycle and apoptosis were tested by CCK-8 assay, wound healing and flow cytometry, respectively. The interaction between FPN and Nrf2 was confirmed by chromatin immunoprecipitation (CHIP) assay.

The viability, migration and mitosis of PC3 cells could be repressed by over-expressed FPN, with decreased intracellular ferritin. The CHIP assay demonstrated that Nrf2 is one transcription factor of FPN and promotes its transcription. With the increase of Nrf2 in PC3 cells, the viability, migration ability and concentration of ferritin were suppressed, while the apoptosis rate was increased. The above effects were counteracted by down-regulating FPN.

FPN could inhibit the prostate cancer cell viability, migration and mitosis, which is also related to a decrease of intracellular ferritin content. In conclusion, Nrf2 suppresses prostate cancer cells viability, migration, and mitosis through upregulating FPN.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 12860

Publication Alerts

Research Papers:

Nuclear transcription factor Nrf2 suppresses prostate cancer cells growth and migration through upregulating ferroportin

Abstract