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The surgical timing after neoadjuvant androgen-deprivation therapy (ADT) plus abiraterone acetate (AA) for patients with locally advanced or metastatic prostate cancer (PCa) is unknown. We divided patients with locally advanced or metastatic PCa into three groups according to prostate-specific antigen (PSA) nadir after neoadjuvant ADT plus AA: group 1 (PSA ≤ 0.2 ng/ml), group 2 (0.2 < PSA ≤ 4.0 ng/ml), and group 3 (PSA > 4.0 ng/ml).The median PSA baseline levels in groups 1, 2, 3 were 118.42 (32.03-457.78), 143.48 (17.7-8100.16), and153.35 (46.44-423.31) ng/ml, respectively. The median times of progression to CRPC in groups 1, 2,and 3 were 30, 26, and 26 months, respectively. Compared to patients with PSA nadir >0.2 ng/ml, patients with PSA nadir <0.2 ng/ml presented with longer PFS (p = 0.048).Our results suggested that, in patients with locally advanced or metastatic PCa, the time to progression to CRPC was longer after radical prostatectomy when PSA decreased below 0.2 ng/ml using neoadjuvant ADT plus AA., (© 2022 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)

Sperm-associated antigen 9 (SPAG9) is closely related to the growth and metastasis of advanced prostate cancer. Docetaxel (DTX) is the gold standard for chemotherapy of prostate cancer, but its side effects decrease the life quality of patients. Therefore, it is urgent to develop combination therapy to increase chemotherapy efficacy for advanced prostate cancer. Oncolytic adenovirus carrying a short hairpin RNA (shRNA) targeting SPAG9 (ZD55-shSPAG9) was applied alone or in combination with docetaxel in prostate cancer cells. Cells were analyzed by cell counting kit-8, Hocehst-33258, transwell and western blot analysis. For in vivo experiments, nude mice were loaded with prostate cancer cells. ZD55-shSPAG9 effectively silenced the expression of SPAG9 in prostate cancer cells in vitro and in vivo. The replication of ZD55-shSPAG9 in prostate cancer cells was not affected by docetaxel, but the combined use of ZD55-shSAPAG9 and docetaxel has a better inhibitory effect on tumor growth and invasion in vitro and in vivo. Our study showed that the combined use of ZD55-shSPAG9 and docetaxel may be a new approach to the treatment of advanced prostate cancer., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Prostate cancer is the second most common malignant tumor in the world, with an incidence rate of 13.5% and a mortality rate of 6.7%. At present, treatment methods for prostate cancer include surgical treatment, endocrine therapy, chemotherapy, and radiotherapy. However, the efficacy of these treatments is not optimal, especially for advanced metastatic prostate cancer. Oncolytic virus has emerged as a novel therapeutic approach for cancer treatment due to its unique advantages such as high selectivity, high efficiency, and low toxicity. The replication ability of oncolytic virus in normal cells is low, while the virus can multiply specifically in tumor cells, which are lysed by the proliferation of the virus, and the induction of apoptosis. In addition, the released progeny virus can infect the surrounding tumor cells and eventually kill the tumor. In this review, we summarize the state-of-the-art progresses and propose new avenues in the development and application of oncolytic virus for the treatment of prostate cancer.

New biomarkers for early diagnosis and prognosis are important in improving the diagnosis of metastatic or recurrent prostate cancer. Recent studies have shown important roles of long non-coding RNAs (lncRNAs) in tumorigenesis. Here we provide a comprehensive review of lncRNAs implicated in prostate cancer and discuss their potential as novel biomarkers and therapeutic targets for prostate cancer. In particular, we focus on lncRNAs associated with the androgen/androgen receptor pathway and the epithelial-to-mesenchymal transition. Notably, several lncRNAs such as PCA3, PCAT18, HOTAIR, and CCAT2 are prostate cancer-specific in that they are only upregulated in prostate cancer, and consequently they are promising biomarkers for use in clinical practice.

In recent years, with the westernization of lifestyle, reduced physical activity and increased prostate-specific antigen (PSA) testing, the incidence of prostate cancer (PCa) has risen significantly in developing countries. Currently, PSA is the only PCa biomarker applied clinically, but it does not perform well in the early diagnosis and distinguishing between benign prostatic hyperplasia and prostate cancer. With the advances in deep sequencing technology, a series of new PCa biomarkers have been recently proposed to improve the diagnostic value of PSA, such as prostate cancer antigen 3 (PCA3), TMPRSS2-ETS fusion gene, microRNA, and other regulatory non-coding RNAs. In addition, the prostate health index (PHI) has been approved by the U.S. Food and Drug Administration (FDA) for clinical use in the detection of PCa. The prostate-specific membrane antigen (PSMA) has been confirmed to be specifically expressed on the surface of PCa cells. In this review, we provide an updated summary of the value and features of these novel biomarkers in the diagnosis and treatment of PCa.

Background: Special AT-rich sequence binding protein 1 (SATB1) is a nuclear factor that functions as the global chromatin organizer to regulate chromatin structure and gene expression gene expression. SATB1 has been shown to be abnormally expressed in various types of cancer. However, the expression and role of SATB1 in prostate cancer remain unclear., Methods: 120 cases of prostatic carcinoma and 60 cases of benign prostate hyperplasia were analyzed for SATB1 expression by immunohistochemistry. LNCaP, DU-145, and PC3 prostate cancer cells were examined for SATB1 expression by Western blot analysis. Cell proliferation and invasion was evaluated by CCK8 and transwell invasion assay, respectively., Results: SATB1 staining was stronger in prostatic carcinomas with metastasis than in those without metastasis, but was absent in benign prostate hyperplasia. Furthermore, SATB1 expression was positively correlated with bone metastasis and the Gleason score. SATB1 overexpression promoted the proliferation and invasion of LNCaP cells while SATB1 knockdown inhibited the proliferation and invasion of DU-145 cells., Conclusions: These findings provide novel insight into oncogenic role of SATB1 in prostate cancer, suggesting that SATB1 is a promising biomarker and therapeutic target for prostate cancer.