کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8330524 1540239 2015 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Overexpression of PDZ-binding kinase confers malignant phenotype in prostate cancer via the regulation of E2F1
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Overexpression of PDZ-binding kinase confers malignant phenotype in prostate cancer via the regulation of E2F1
چکیده انگلیسی
Roles and mechanisms of cell cycle-specific transcription factor E2F1 on prostate cancer (PCa) have not been fully elucidated. To address this problem, we here identified PDZ-binding kinase (PBK) as a direct target for E2F1 through bioinformatics binding site prediction, combined with chromatin immunoprecipitation-PCR (ChIP-PCR), quantitative (Q)-PCR and Western blot analysis. Then, we observed that the knockdown of both E2F1 and PBK could suppress cell proliferation, invasion and migration of PCa cell lines in vitro. Based on Taylor dataset, we found that PBK upregulation occurred more frequently in PCa patients with the older age of patients (P = 0.044), the higher Gleason score (P < 0.001), the advanced clinical pathological stage (P = 0.019), the presence of metastasis (P = 0.008), the overall survival (P < 0.001) and PSA failure (P = 0.004). More interestingly, the survival analysis identified PBK as an independent factor for predicting the biochemical recurrence-free survival of PCa patients (P = 0.041). Taken together, these findings offer the convincing evidence for the first time that the overexpression of PBK may lead to high malignant phenotype in PCa cells via the regulation of E2F1. PBK may function as a biomarker that can differentiate patients with biochemical recurrent and non-biochemical recurrent disease following radical prostatectomy, highlighting its potential as a therapeutic target.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Journal of Biological Macromolecules - Volume 81, November 2015, Pages 615-623
نویسندگان
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