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Epithelial mesenchymal transition (EMT) is a process of normal cell physiological development, in which epithelial cells transform into mesenchyme cells through a specific program. EMT plays a key role in inflammatory reaction, cell development, tumor invasion, and metastasis and has an interrelation with prostate cancer stem cells. Recent researches show the involvement of EMT in the development and metastasis of prostate cancer. This article reviews the specific roles and action mechanisms of EMT in the progression of prostate cancer.

Testicular nuclear receptor 4 (TR4) plays protective roles against oxidative stress and DNA damage and might contribute to aging. Our recent clinical tumor tissue staining results showed higher expression of TR4 in prostate cancer (PCa) patients with high Gleason scores compared to the tissues with the low Gleason scores. In vitro migration/invasion assays after manipulation of the TR4 expression in PCa cells showed that TR4 promoted PCa cells migration/invasion. Mechanism dissection found that the CCL2/CCR2 signal plays the key role in the mediation of TR4-promoted PCa cells migration/invasion. Chromatin immunoprecipitation and Luciferase assays further confirmed TR4 modulation of CCL2 at the transcriptional level and addition of the CCR2 antagonist led to interruption of the TR4-enhanced PCa cells migration/invasion. Finally, the orthotopic xenografted mice studies using the luciferase expressing CWR22Rv1 cells found that TR4 enhanced PCa metastasis and this increased metastasis was reversed when the CCR2 antagonist was injected into the mice. Together, these in vitro and in vivo results revealed a positive role of TR4 in PCa metastasis and demonstrated CCL2/CCR2 signaling as an important mediator in exerting TR4 action. This finding suggests that TR4 may represent a biomarker related to PCa metastasis and targeting the TR4-CCL2/CCR2 axis may become a new therapeutic approach to battle PCa metastasis., (© 2014 UICC.)

Background: DNA damage, caused by numerous carcinogens, contributes to the increased risk of different types of cancer. The base excision repair (BER) pathway including the apurinic/apyrimidic endonuclease (APE1, also known as APEX1) gene plays an important role in preventing the accumulation of DNA damage and maintaining genomic stability. The aim of the present study is to determine whether polymorphisms of APE1 are associated with the risk of prostate cancer (PCa) in the Chinese Han population., Methods: This study consisted of 198 patients with PCa and 156 healthy controls. The polymorphisms of APE1, Asp148Glu (rs1130409) and -141T/G (rs1760944) were determined by the polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) method., Results: The genotypic distributions of the two polymorphisms in controls were in Hardy-Weinberg equilibrium (p = 0.92 and p = 0.83, respectively). Logistic regression analysis indicated that the -141GG genotype was significantly associated with a decreased risk of PCa compared with the -141TT genotype (p = 0.03; OR 0.49; 95% CI 0.26 - 0.92). The G allele was also significantly associated with a reduced risk of PCa compared with the T allele (p = 0.02; OR 0.71; 95% CI 0.52 - 0.96). However, no association between Asp148Glu polymorphism and the risk of PCa was found., Conclusions: The -141GG genotype and G allele of the APE1 gene are associated with a decreased risk of PCa in the Chinese Han population.

Objective: To investigate the clinical presentation, pathologic features, treatment and prognosis of prostatic paraganglioma., Methods: We retrospectively studied a case of prostatic paraganglioma and reviewed relevant literature. The patient was a 39-year-old man, admitted for repeated hematospermia for over 12 months. After misdiagnosed as having prostate cancer, he underwent suprapubic prostatectomy, with the tumor completely removed., Results: Postoperative pathological examination confirmed the tumor to be prostatic paraganglioma, which was non-functional, with the immunohistochemical results of NSE (+), CGA (+), S100 (+), CK (-) and Desmin (-). Postoperative blood pressure was stable. Two weeks after surgery, the urethral catheter was removed and the patient discharged. No recurrence was found during 48 months of follow-up., Conclusion: Lacking specific clinical characteristics, paraganglioma of the prostate is easily misdiagnosed, and can be confirmed only by postoperative pathology and immunohistochemistry. For the treatment of this rare tumor, little experience has been accumulated, and further studies are needed.

Objective: To investigate the clinical presentations and pathologic features of undifferentiated sarcoma of the prostate with cartilage metaplasia, and to clarify its category., Methods: We analyzed the clinical data of a case of undifferentiated sarcoma of the prostate with cartilage metaplasia treated by surgical resection. The tumor tissue was subjected to routine HE and immunohistochemical staining, its histological structure and immunohistochemical expression were observed under the light microscope, and relevant literature on its manifestations was reviewed., Results: The case was pathologically diagnosed as gray prostate tumor, with chondrosarcomatous and undifferentiated malignant mesenchymal components under the light microscope. Immunohistochemical staining revealed vimentin (+), local CD117 (+/-), SMA (-), Des (-), myoglobin (-), CD34 (-), CK7 (-), and CK8 (-). Tumor metastasis was found 2 months after the operation, and the patient died 4 months later., Conclusion: Undifferentiated sarcoma of the prostate with cartilage metaplasia is a very rare and highly malignant aggressive tumor, which can be diagnosed by biopsy and immunohistochemistry.

Objective: To study the clinical manifestations, pathological characteristics and treatment methods of prostate cancer with five different histological features., Methods: We reported 1 case of prostate cancer with five different histological features and further analyzed the diagnosis, pathology and treatment of the disease by reviewing the relevant literature., Results: The patient was an 84-year-old male, admitted due to difficult urination and dribbling urine for 1 year, hematuria for 8 months and deterioration for 2 weeks. Prostate cancer was indicated by rectal examination, ultrasonography, CT, MRI and PSA, and confirmed by biopsy. Considering the general condition of the patient, we performed electrotransurethral resection under epidural anesthesia to alleviate his urinary symptoms and remove suspected tumor tissues. Postoperative pathology showed the case to be prostate adenocarcinoma, histologically characterized by cribriform carcinoma, acinar carcinoma, diffuse invasive carcinoma, ductal carcinoma, and mucinous adenocarcinoma, with a Gleason score of 9. Bicalutamide and goserelin were administered postoperatively. Systemic metastasis occurred 10 months later, and the patient died 1 year after the operation., Conclusion: Prostate cancer with five different histological features is extremely rare. Its early diagnosis is difficult and mainly depends on pathological and immunohistochemical examinations, and radical prostatectomy can be considered for its treatment.

Aim: To examine the physiological role of the androgen receptor (AR) in the PC-3 cell line by transfecting full-length functional AR cDNA driven by its natural human AR promoter., Methods: We generated an AR-expressing PC-3(AR)9 stable clone that expresses AR under the control of the natural human AR promoter and compared its proliferation to that of the PC-3(AR)2 (stable clone that expresses AR under the control of the cytomegalovirus (CMV) promoter, established by Heisler et al.) after androgen treatment., Results: We found that dihydrotestosterone (DHT) from 0.001 nmol/L to 10 nmol/L induces cell cycle arrest or inhibits proliferation of PC-3(AR)2 compared with its vector control, PC-3(pIRES). In contrast, PC-3(AR)9 cell growth slightly increased or did not change when treated with physiological concentrations of 1 nmol/L DHT., Conclusion: These data suggest that intracellular control of AR expression levels through the natural AR promoter might be needed for determining AR function in androgen-independent prostate cancer (AIPC) PC-3 cells. Unlike previous publications that showed DHT mediated suppression of PC-3 growth after transfection of viral promoter-driven AR overexpression, we report here that DHT-mediated PC-3 proliferation is slightly induced or does not change compared with its baseline after reintroducing AR expression driven by its own natural promoter, as shown in PC-3(AR)9 prostate cancer cells.