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Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells
المؤلفون المشاركون
Chen, Kun
Xu, Houqiang
Zhao, Jiafu
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-19، 19ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-05-09
دولة النشر
مصر
عدد الصفحات
19
التخصصات الرئيسية
الملخص EN
Purpose.
Prostate cancer (PC) is a common malignant tumor and a leading cause of cancer-related death in men worldwide.
In order to design new therapeutic interventions for PC, an understanding of the molecular events underlying PC tumorigenesis is required.
Bloom syndrome protein (BLM) is a RecQ-like helicase, which helps maintain genetic stability.
BLM dysfunction has been implicated in tumor development, most recently during PC tumorigenesis.
However, the molecular basis for BLM-induced PC progression remains poorly characterized.
In this study, we investigated whether BLM modulates the phosphorylation of an array of prooncogenic signaling pathways to promote PC progression.
Methods.
We analyzed differentially expressed proteins (DEPs) using iTRAQ technology.
Site-directed knockout of BLM in PC-3 prostate cancer cells was performed using CRISPR/Cas9-mediated homologous recombination gene editing to confirm the effects of BLM on DEPs.
PathScan® Antibody Array Kits were used to analyze the phosphorylation of nodal proteins in PC tissue.
Immunohistochemistry and automated western blot (WES) analyses were used to validate these findings.
Results.
We found that silencing BLM in PC-3 cells significantly reduced their proliferative capacity.
In addition, BLM downregulation significantly reduced levels of phosphorylated protein kinase B (AKT (Ser473)) and proline-rich AKT substrate of 40 kDa (PRAS40 (Thr246)), and this was accompanied by enhanced ROS (reactive oxygen species) levels.
In addition, we found that AKT and PRAS40 inhibition reduced BLM, increased ROS levels, and induced PC cell apoptosis.
Conclusions.
We demonstrated that BLM activates AKT and PRAS40 to promote PC cell proliferation and survival.
We further propose that ROS act in concert with BLM to facilitate PC oncogenesis, potentially via further enhancing AKT signaling and downregulating PTEN expression.
Importantly, inhibiting the BLM-AKT-PRAS40 axis induced PC cell apoptosis.
Thus, we highlight new avenues for novel anti-PC treatments.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Chen, Kun& Xu, Houqiang& Zhao, Jiafu. 2019. Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-19.
https://search.emarefa.net/detail/BIM-1203357
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Chen, Kun…[et al.]. Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-19.
https://search.emarefa.net/detail/BIM-1203357
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Chen, Kun& Xu, Houqiang& Zhao, Jiafu. Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-19.
https://search.emarefa.net/detail/BIM-1203357
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1203357
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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