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Asparaginyl endopeptidase promotes proliferation and invasiveness of prostate cancer cells via PI3K/AKT signaling pathway

Zhu, Wenjing, Shao, Yiqun, Yang, Ming, Jia, Moran, Peng, Yu
Gene 2016 v.594 no.2 pp. 176-182
apoptosis, cell proliferation, gene expression regulation, metastasis, neoplasm cells, prostatic neoplasms, signal transduction, staining, therapeutics
Recurrence and metastasis are the major lethal causes of prostate cancer. It is urgent to find out the mechanisms and key factors governing prostate cancer progression and metastasis for developing new therapeutic strategies. Asparaginyl endopeptidase (AEP) overexpression has been found in a number of solid tumors. In prostate cancer, AEP has also been shown to exhibit a vesicular staining pattern and significantly associated with advanced tumor stage, high Gleason score, perineural invasion, and larger tumor. Here, we found that AEP was differentially expressed in prostate cancer cells with higher expression in 22RV1 cells and lower expression in PC-3 cells. AEP knockdown in 22RV1 cells significantly inhibited cell proliferation and invasion abilities while overexpression of AEP in PC-3 cells prompted cell proliferation and invasion abilities. Meanwhile, AEP knockdown upregulated cell apoptosis and vice versa. Further, we firstly identified that AEP promotes activation of the PI3K-AKT signaling pathway in prostate cancer cells. Taken together, our results suggest that AEP may be an attractive target for prostate cancer therapy.