Nuclear transcription factor Nrf2 suppresses prostate cancer cells growth and migration through upregulating ferroportin
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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
Xiaozhou He, email: email@example.com
Keywords: prostate cancer, ferroportin, Nrf2, ferritin, apoptosis
Received: July 29, 2016 Accepted: October 04, 2016 Published: October 24, 2016
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.
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