IRF5 inhibits prostate cancer metastasis and drug resistance by decreasing CXCR4/CXCL12 complex
Öz
Purpose: Prostate cancer is the most common type of cancer in men, and drug resistance is typical in its treatment. Chemokines especially play a role in tumor growth and drug resistance mechanisms. IRF5 is a critical transcription factor in immune response, and its relationship with the chemokine family CXCR4 and CXCL12 was investigated in this study.
Materials and Methods: The pIRF5 plasmid was transfected in an androgen-independent human prostate cancer cell line (PC3), and the IRF5 protein was overexpressed. CXCR4 and CXCL12 protein expression levels were determined by western blot and gene expression levels by the qPCR method. In addition, colony formation was examined in cells after IRF5 transfection, and CXCL12 secretion was measured in cell media.
Results: Cell viability and colony formation were found to be significantly reduced in IRF5 transfected PC3 cells. In addition, CXCR4 and CXCL12 protein expression and gene expression levels of IRF5 transfected cells were found to be significantly decreased.
Conclusion: This study shows that IRF5, a transcription factor, affects CXCR4/CXCL12, which is involved in microenvironment-mediated metastasis developing in prostate cancer. Thus, in the treatment of prostate cancer, IRF5 gene therapy can prevent metastasis and offer essential contributions to newly developed treatment methods in this regard.
Anahtar Kelimeler
Destekleyen Kurum
Adnan Menderes University Research Grant Projects
Proje Numarası
TPF-19021
Teşekkür
This work was supported by the Adnan Menderes University Research Grant Projects (TPF-19021) and by a grant (214Z057) from the Scientific and Technological Research Council of Turkey (TUBITAK) to Dr. Ozge Cevik.
Kaynakça
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