RecQ helicase BLM regulates prostate cancer cell proliferation and apoptosis

Qian,Xiaosong; Feng,Sujuan; Xie,Dawei; Feng,Dalin; Jiang,Yihang; Zhang,Xiaodong

doi:10.3892/ol.2017.6704

RecQ helicase BLM regulates prostate cancer cell proliferation and apoptosis

Authors:
- Xiaosong Qian
- Sujuan Feng
- Dawei Xie
- Dalin Feng
- Yihang Jiang
- Xiaodong Zhang
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Affiliations: Institute of Uro‑Nephrology, Beijing Chao‑Yang Hospital, Capital Medical University, Beijing 100020, P.R. China
Published online on: August 2, 2017 https://doi.org/10.3892/ol.2017.6704
Pages: 4206-4212
Copyright: © Qian et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Prostate cancer (PCa) is a common malignant tumor and the second leading cause of morbidity and mortality in men worldwide. Considering the prevalence and effects of PCa in males, an understanding of the molecular mechanisms underlying PCa tumorigenesis are essential and may provide novel therapeutic strategies for treating PCa. Bloom syndrome protein (BLM) is a member of the RecQ helicase family. The major function of BLM is to uncoil the double‑stranded DNA structure. It has previously been demonstrated that BLM acts as a ‘genome caretaker’, and dysregulation of BLM function has been implicated in the development of multiple tumor types; however, its potential for inducing PCa tumorigenesis remains undetermined. The present study aimed to explore the function of BLM in PCa progression. Reverse transcription‑polymerase chain reaction, immunohistochemistry and western blot analyses were performed to detect the BLM expression pattern in PCa patients and cell lines. The proliferation, and migration and invasion capacities of prostate cells were determined by EdU and Transwell assays following transfection with BLM‑targeting short hairpin RNA (shRNA). The expression of BLM was significantly increased in PCa tissues and PC3 cells compared with non‑PCa tissues and benign prostatic hyperplasia cells. Knockdown of BLM via shRNA inhibited PCa cell proliferation, and promoted PCa cell apoptosis. Notably, reducing the expression of BLM had no effect on the migration or invasive abilities of PCa cells. These results suggest that downregulation of BLM may alleviate PCa development, providing a novel perspective for PCa tumorigenesis and a potential therapeutic target for PCa.

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