Consecutive Prostate Cancer Specimens Revealed Increased Aldo-Keto Reductase Family 1 Member C3 Expression with Progression to Castration-Resistant Prostate Cancer
Consecutive Prostate Cancer Specimens Revealed Increased Aldo-Keto Reductase Family 1 Member C3 Expression with Progression to Castration-Resistant Prostate Cancer
复制标题
连续前列腺癌标本显示醛酮还原酶家族 1 成员 C3 表达增加，并进展为去势抵抗性前列腺癌
DOI：
10.3390/jcm8050601
复制
发表时间：
2019-05-01
影响因子：
3.9
通讯作者：
Inoue, Takahiro
中科院分区：
文献类型：
--
作者：
Miyazaki, Yu;Teramoto, Yuki;Inoue, Takahiro
醛酮还原酶家族1成员C3（AKR1C3）是类固醇生成途径中的酶，特别是在睾酮和二氢睾酮的形成中，并且被认为在促进前列腺癌（PCa）进展，特别是在去势抵抗性前列腺癌（CRPC）中具有关键作用。本研究旨在比较AKR1C3在良性前列腺上皮和癌细胞之间以及在来自同一患者的未经治疗的前列腺癌（HNPC）和CRPC之间的表达水平，以了解AKR1C3在PCa进展中的作用。对134例乳腺癌组织中AKR1C3的表达进行相关性分析。此外，分析了AKR1C3表达与根治性前列腺切除术后前列腺特异性抗原（PSA）无进展生存期（PFS）之间的相关性。此外，我们评估了来自11名患者的连续前列腺样本，这些患者均处于去势初治和去势抵抗状态。在局限性HNPC患者中，癌上皮的AKR1C3免疫染色显著强于良性上皮（p < 0.0001）。AKR1C3高表达是PSA PFS差的独立因素（p = 0.032）。此外，在相同患者中，CRPC组织中的AKR1C3免疫染色显著强于HNPC组织（p = 0.0234）。我们的研究结果表明AKR1C3在PCa进展中至关重要。
Aldo-keto reductase family 1 member C3 (AKR1C3) is an enzyme in the steroidogenesis pathway, especially in formation of testosterone and dihydrotestosterone, and is believed to have a key role in promoting prostate cancer (PCa) progression, particularly in castration-resistant prostate cancer (CRPC). This study aims to compare the expression level of AKR1C3 between benign prostatic epithelium and cancer cells, and among hormone-naive prostate cancer (HNPC) and CRPC from the same patients, to understand the role of AKR1C3 in PCa progression. Correlation of AKR1C3 immunohistochemical expression between benign and cancerous epithelia in 134 patient specimens was analyzed. Additionally, correlation between AKR1C3 expression and prostate-specific antigen (PSA) progression-free survival (PFS) after radical prostatectomy was analyzed. Furthermore, we evaluated the consecutive prostate samples derived from 11 patients both in the hormone-naive and castration-resistant states. AKR1C3 immunostaining of cancer epithelium was significantly stronger than that of the benign epithelia in patients with localized HNPC (p < 0.0001). High AKR1C3 expression was an independent factor of poor PSA PFS (p = 0.032). Moreover, AKR1C3 immunostaining was significantly stronger in CRPC tissues than in HNPC tissues in the same patients (p = 0.0234). Our findings demonstrate that AKR1C3 is crucial in PCa progression.