Expression of spermidine/spermine N(1) -acetyl transferase (SSAT) in human prostate tissues is related to prostate cancer progression and metastasis.
Expression of spermidine/spermine N(1) -acetyl transferase (SSAT) in human prostate tissues is related to prostate cancer progression and metastasis.
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DOI：
10.1002/pros.22996
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发表时间：
2015-08-01
期刊：
影响因子：
2.8
通讯作者：
Basu, Hirak S.
中科院分区：
文献类型：
--
作者：
Huang, Wei;Eickhoff, Jens C.;Mehraein-Ghomi, Farideh;Church, Dawn R.;Wilding, George;Basu, Hirak S.
PCa in many patients remains indolent for the rest of their lives, but in some patients it progresses to lethal metastatic disease. Gleason Score (GS) is the current clinical method for PCa prognosis. It cannot reliably identify aggressive PCa, when GS is ≤7. It is shown that oxidative stress plays a key role in PCa progression. We have shown that in cultured human PCa cells, an activation of Spermidine/Spermine N1-acetyl transferase (EC 2.3.1.57) enzyme initiates a polyamine oxidation pathway and generates copious amounts of reactive oxygen species (ROS) in polyamine-rich PCa cells. We used RNA in situ hybridization (RNA-ISH) and immunohistochemistry (IHC) methods to detect SSAT mRNA and protein expression in two tissue microarrays (TMA) created from patient prostate tissues. We analyzed 423 patient prostate tissues in the two TMAs. Our data show that there is a significant increase in both SSAT mRNA and the enzyme protein in the PCa cells as compared to their benign counterpart. This increase is even more pronounced in metastatic PCa tissues as compared to the PCa localized in the prostate. In the prostatectomy tissues from early-stage patients, the SSAT protein level is also high in the tissues obtained from the patients who ultimately progress to advanced metastatic disease. Based on these results combined with published data from our and other laboratories we propose an activation of an autocrine feed-forward loop of PCa cell proliferation in the absence of androgen as a possible mechanism of castrate-resistant prostate cancer (CRPCa) growth.
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