Expression In Benign Prostatic Hyperplasia Research Articles

The study of Mucin stains and Cyclin D1 expression in benign prostatic hyperplasia and prostatic adenocarcinoma (Immunohistochemical study)

The study of Mucin stains and Cyclin D1 expression in benign prostatic hyperplasia and prostatic adenocarcinoma (Immunohistochemical study)

Upregulation of mir-1199-5p is associated with reduced type 2 5-α reductase expression in benign prostatic hyperplasia

Background5-α reductase inhibitors (5-ARIs) are first-line drugs for managing benign prostatic hyperplasia (BPH). Unfortunately, some patients do not respond to 5-ARI therapy and may even show worsening symptoms. The decreased expression of steroid 5-α reductase type 2(SRD5A2) in BPH tissues may explain the failure of 5-ARI therapy, however, the mechanisms underlying SRD5A2 decreased remained unelucidated.ObjectivesTo investigate microRNA-mediated regulation of the expression of SRD5A2 resulting in 5-ARI therapy failure.Materials and methodsThe expression of SRD5A2 and microRNAs in BPH tissues and prostate cells were detected by immunohistochemistry, western blotting, and quantitative real-time PCR. Dual-luciferase reporter assay was performed to confirm that microRNA directly combine to SRD5A2 mRNA. The apoptosis of prostatic cells was detected by flow cytometry.ResultsSRD5A2 expression was variable; it was negative, weak, and strong in 13.6%, 28.8%, and 57.6% of BPH tissues respectively. The normal human prostatic epithelial cell line RWPE-1 strongly expressed SRD5A2, whereas the immortalized human prostatic epithelial cell line BPH-1 weakly expressed SRD5A2. miR-1199-5p expression was remarkably higher in BPH-1 than in RWPE-1 cells(P<0.001), and miR-1199-5p expression was significantly upregulated in BPH tissues with negative SRD5A2 expression than those with positive SRD5A2 expression. Transfection of miR-1199-5p mimics in RWPE-1 cells led to a marked decrease in SRD5A2 expression, whereas miR-1199-5p inhibitor increased SRD5A2 expression in BPH-1 cells. Dual-luciferase reporter assay showed that miR-1199-5p could bind the 3′untranslated region of SRD5A2 mRNA. miR-1199-5p also decreased the RWPE-1 sensibility to finasteride, an inhibitor of SRD5A2.ConclusionOur results show that SRD5A2 expression varies in BPH tissues and miR-1199-5p might be one of the several factors contributing to differential SRD5A2 expression in BPH patients.

Clinicopathological correlation of p53 expression in benign prostatic hyperplasia and prostate adenocarcinoma

Prostate adenocarcinoma is the 6 most common carcinoma in men worldwide. It is usually a cancer of the elderly age group. Benign prostatic hyperplasia is a common cause of urinary incontinence and urine flow symptoms, usually seen in the middle along with elderly age group. In this study we have evaluated the expression of p53 immunohistochemistry (IHC) in prostate adenocarcinoma with benign prostatic hyperplasia along with its diagnostic, treatment and prognostic implications.: 1. Assessment of clinical and biochemical parameters in patients with benign prostatic hyperplasia (BPH) and prostate adenocarcinoma. 2. To assess p53(IHC) expression in benign prostatic hyperplasia and prostate adenocarcinoma : The study population comprised of a subset of patients who came to Ramaiah hospital, Bangalore from May 2018 till June 2019, for treatment regarding prostate related symptoms. The clinicodemographic data was collected and prostate biopsies were taken for which histopathological assessment was done. A total of 60 cases comprising of 30 cases of BPH and 30 cases of prostatic adenocarcinoma was subjected to p53 immunohistochemistry. The results were tabulated and statistically analyzed for significance.The present prospective study was conducted on 60 patients with 30 cases (50%) of BPH and 30 cases (50%) of prostatic adenocarcinoma. Based on the tumor differentiation there was 1 case (3.3%) of well differentiated carcinoma, 18 cases(60%) of moderately differentiated carcinoma and 11cases (36.6%) of poorly differentiated carcinomas. We observed an inverse relationship between p53 expression and histological grade. All poorly differentiated carcinoma had higher p53(&amp;#62;50% expression). There was statistically significant difference in expression of p53 between cases of BPH and carcinoma prostate, indicated by P value of &amp;#60;0.05. Among prostate carcinomas p53 had higher expression on those cases with Gleason score 9 and 10.: P53 expression directly correlates with Gleason score, while inversely correlating with tumor differentiation of prostate carcinoma cases. The expression of p53 is low in BPH as compared to that of prostate cancers. Hence it can be used as a good diagnostic and prognostic marker in prostate carcinoma.

LIM domain kinase 1

Background Despite recent advancement, prostate cancer (PC) remains to represent a leading cause of cancer mortality and morbidity in men. Diagnosis of PC faces many challenges, especially on core biopsies. Multiple signaling pathways have been involved in PC progression. However, castration resistance eventually develops, especially in metastatic PC. Identifying a marker that helps in distinguishing invasive tumor from benign and precursor lesions, as well as predicts its metastatic and prognostic potentials, is needed. LIM-domain kinase 1 (LIMK1) is a newly identified marker that affects the cytoskeleton of cancer cells. Its role in PC is still not well understood. This study aimed at evaluating LIMK1 expression in benign prostatic hyperplasia (30 cases), high-grade prostatic intraepithelial neoplasia (27 cases), and PC prostatic adenocarcinoma (60 cases) and its association with the prognostic clinicopathological parameters in PC. Results No strong expression was detected in benign prostatic hyperplasia expression compared with 25.9% and 48.3% in high-grade prostatic intraepithelial neoplasia and prostatic adenocarcinoma (Pca) groups. The expression was statistically higher in the Pca group than the other groups. There was significant association with poor prognostic parameters in Pca groups, including higher prostate-specific antigen levels, tumor percentage, Gleason scores, grade groups, T stage, positive lymph-node metastases, extracapsular extension, seminal vesicle invasion, distant metastasis, and prognostic-stage group. Conclusion LIMK1 is considered a promising diagnostic and prognostic marker in Pca.

AKR1B10 expression in benign prostatic hyperplasia and its related mechanism.

The aim of the present study was to investigate the expression of aldo-keto reductase family 1 member B10 (AKR1B10) in benign prostatic hyperplasia (BPH) and its related mechanism. In total, 142 BPH patients admitted from March 2017 to March 2019 at the First Hospital of Hunan University of Chinese Medicine and 140 healthy people undergoing physical examination were selected as the research subjects. The clinical value of AKR1B10 in BPH was analyzed. Twenty clean SD rats were selected, and 10 were selected to establish the prostate hyperplasia model, while the remaining 10 were set as the control group. Ten days after the model was established, AKR1B10 and NF-κB expression in prostate tissues of rats in both groups was detected by PCR and immunohistochemistry. The primary cells in prostate hyperplasia were cultured, and then they were transfected with AKR1B10 to observe the changes of cell biological behavior. AKR1B10 and NF-κB mRNA significantly increased in peripheral blood of BPH patients and prostate tissue of BPH model rats (P<0.001), and AKR1B10 had good diagnostic value for BPH (P<0.001). In addition, it was positively correlated with PSA, EGF, IL-6 and TNF-α (P<0.001). After transfection with AKR1B10-inhibitor, it was revealed that the proliferation of prostate hyperplasia cells decreased, while the apoptosis of prostate hyperplasia cells increased and the NF-κB protein expression decreased (P<0.001). Collectively, high expression of AKR1B10 in BPH promoted the proliferation of prostate cells and reduced their apoptosis, and the mechanism may be through regulation of NF-κB.

Abstract PR09: MicroRNA-1205 regulation of FRYL and aggressive prostate cancer in men of African ancestry

Abstract Men of African ancestry (moAA) have increased likelihood for development of aggressive prostate cancer (PCa). PCa deaths are often associated with castration-resistant prostate cancer (CRPC) due to maintenance of androgen receptor (AR) signaling in PCa cells following androgen ablation therapy (ADT). The 8q24 chromosomal locus is a highly susceptible PCa region that carries risk genetic variants associated with increased incidence of aggressive PCa in moAA. This region also carries frequent amplifications of the PVT1 gene, a nonprotein coding gene that encodes microRNA-1205 whose function was previously unknown. We examined miR-1205 mRNA expression in a cohort of normal (n=22), benign prostatic hyperplasia (n=42), and PCa (n=26) histologically confirmed prostatic tissues obtained from prostatectomy or transrectal biopsies of moAA in Ibadan, Nigeria. A Tukey post hoc test revealed decreased miR-1205 expression in benign prostatic hyperplasia (4.61 ± 7.5) and PCa (3.39 ± 3.53) when compared to normal tissues (6.55 ± 9.5), suggesting that miR-1205 may function as a tumor suppressor and loss of miR-1205 is characteristic of PCa in moAA. In vitro studies revealed decreased miR-1205 expression in CRPC (C4-2B and 22RV1) cells when compared to non-CRPC (LNCaP) cells, suggesting a role for miR-1205 in CRPC. Furthermore, we observed significant inhibition of tumor growth in NOD/SCID gamma mice implanted with C4-2B cells that were administered our novel synthetic analog of miR-1205 (patent pending) when compared to mice treated with a scramble oligonucleotide, indicating that miR-1205 can suppress CRPC tumors. We identified Fry-like (FRYL) as a putative target of miR-1205 using a miSVR computer algorithm and subsequently observed FRYL and AR overexpression in prostate tumors compared to normal tissue from fourteen PCa patients when whole-transcriptome analysis was performed using the Galaxy web platform. Moreover, FRYL was overexpressed in CRPC cells when compared with non-CRPC cells, further suggesting a role in CRPC development. C4-2B cells transfected with miR-1205 and the 3′ UTR of FRYL in a luciferase expressing vector revealed a significant decrease in luciferase activity when compared to control cells, indicating direct binding of miR-1205 to the 3′ UTR of FRYL. These observations strongly suggest that miR-1205 acts as a tumor suppressor by directly targeting FRYL mRNA in PCa cells. FRYL is predicted to regulate dendritic branching, leading to our hypothesis that FRYL plays a role in the development of PCa with neuroendocrine differentiation (PCND), a resulting mechanism due to ADT resistance. We observed that FRYL mRNA was overexpressed and miR-1205 was significantly underexpressed after fourteen days of inducing PCND in LNCaP cells, suggesting that miR-1205 regulation of FRYL mRNA may play a role in PCND development. Further understanding miR-1205 regulation of FRYL may provide novel insights into the molecular mechanisms of aggressive PCa. This abstract is also being presented as Poster B068. Citation Format: Michelle K. Naidoo, Fayola Levine, Tamara Gillot, Thahmina Ali, Konstantinos Krampis, Akintunde Orunmuyi, E.O. Olapade-Olaopa, Olorunseun O. Ogunwobi. MicroRNA-1205 regulation of FRYL and aggressive prostate cancer in men of African ancestry [abstract]. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr PR09.

Morphological change and characteristics of myofibroblasts during the growth process of benign prostatic hyperplasia.

To clarify the morphological change and characteristics of myofibroblast during the growth process of benign prostatic hyperplasia. This study examined the characteristics of myofibroblasts during the growth process of the prostate in the stromal component-dominant benign prostatic hyperplasia rat model. Transforming growth factor-β1 and insulin-like growth factor-binding protein3 expression were evaluated by western blotting (n=6). We used double immunohistochemical staining to evaluate the number of myofibroblasts positive for α-smooth muscle actin and vimentin in benign prostatic hyperplasia tissues. Expression and histological analyses of the benign prostatic hyperplasia were also carried out in rats at 2, 3 and 8weeks after urogenital sinus implantation (n=6). To evaluate the fine morphological characteristics of myofibroblasts in human benign prostatic hyperplasia tissues, electron microscopy analysis was additionally carried out. There was a significant upregulation of the transforming growth factor-β1 and insulin-like growth factor-binding protein3 expression in benign prostatic hyperplasia (P<0.05). There was a significant increase in the number of myofibroblasts in benign prostatic hyperplasia (P<0.05) compared with normal prostate, with these abundantly located in the stromal area. The transforming growth factor-β1 and insulin-like growth factor-binding protein3 expression and number of myofibroblasts showed a time-dependent increase (P<0.05), with growth factor expressions preceding the myofibroblast increase. Electron microscopy confirmed that the myofibroblast progenitor cells, which possess abundant stress fibers, were predominantly located around fibrous areas in human benign prostatic hyperplasia. Differentiation into myofibroblasts induced by transforming growth factor-β1 and insulin-like growth factor-binding protein3 actively occurs during the growth process of benign prostatic hyperplasia. Myofibroblast progenitor cells seem to be associated with prostatic fibrosis in human benign prostatic hyperplasia.

The Significance of Aldehyde Dehydrogenase 1A1 Expression in Benign Prostatic Hyperplasia, Prostatic Intraepithelial Neoplasia and Prostatic Adenocarcinoma

Background: Prostatic carcinoma contains a small population of cancer stem cells (CSCs) that promote tumor growth, maintenance, and progression. CSC markers could provide a prognostic tool for human malignancies. Therefore, CSCs may have a role in prostatic carcinoma. This study aimed to evaluate the expression patterns and significance of stem cell marker aldehyde dehydrogenase 1A1 (ALDH1A1) in prostatic adenocarcinoma. Methods: This is a retrospective study performed upon 60 cases grouped as; 10 cases (16.7%) of benign prostatic hyperplasia (BPH), 6 cases (10%) of high-grade prostatic intraepithelial neoplasia (HGPIN) and 44 cases (73.3%) of prostatic adenocarcinoma (PCa) of different Gleason scores. Immunohistochemistry was applied on formalin-fixed, paraffin-embedded blocks using ALDH1A1. The relation between ALDH1A1 expression and clinicopathologic parameters was assessed. Results: Low expression of ALDH1A1 was seen in all cases (100%) of BPH, 5/6 (83.3%) of HGPIN and 12/44 (27.3%) of PCa, while high expression was in 1/6 case (16.7%) of HGPIN and 32/44 (72.2%) of PCa cases. There were significant relations between the expression levels of ALDH1A1 in PCa compared with HGPIN and BPH cases (P<0.01). ALDH1A1 expression showed highly significant associations with pre-operative serum PSA level, Gleason score, Gleason Grade Group (P<0.01) and was significantly associated with perineural invasion and tumor stage (P<0.05). No significant relations were found between ALDH1A1 expression and patients` age, capsular invasion, lymphovascular invasion, depth of invasion (pT) or lymph node metastasis. Conclusion: ALDH1A1 is a prostate CSC marker, could be involved in tumorigenesis and progression of prostatic adenocarcinoma

Androgen receptor isoforms expression in benign prostatic hyperplasia and primary prostate cancer.

The role of molecular changes in the androgen receptor (AR) as AR variants (AR-Vs) is not clear in the pathophysiology of benign prostatic hyperplasia (BPH) and hormone-naïve PCa. The aim of the current work was to identify the presence of AR isoforms in benign tissue and primary PCa, and to evaluate the possible association with tumor aggressiveness and biochemical recurrence in primary PCa. The mRNA levels of full length AR (AR-FL) and AR-Vs (AR-V1, AR-V4 and AR-V7) were measured using RT-qPCR. The protein expression of AR-FL (AR-CTD and AR-NTD) and AR-V7 were evaluated by the H-Score in immunohistochemistry (IHC). All investigated mRNA targets were expressed both in BPH and PCa. AR-FL mRNA levels were similar in both groups. AR-V4 mRNA expression showed higher levels in BPH, and AR-V1 and AR-V7 mRNA expression were higher in PCa. The AR-V7 protein showed a similar H-Score in both groups, while AR-CTD and AR-NTD were higher in nuclei of epithelial cells from BPH. These results support the assumption that these constitutively active isoforms of AR are involved in the pathophysiology of primary PCa and BPH. The role of AR-Vs and their possible modulation by steroid tissue levels in distinct types of prostate tumors needs to be elucidated to help guide the best clinical management of these diseases.

A proteomic glimpse into the oncogenesis of prostate cancer

Prostate cancer (PCa) is the second most frequent cancer in men worldwide. Distinguishing between the nonaggressive and aggressive forms of this disease is difficult, and a means to better characterize molecular patterns that could aid in diagnosis is urgently needed. Here, we compare the proteomic profiles of PCa and benign prostatic hyperplasia (BPH) in an effort to elucidate underlying mechanisms of oncogenesis. We compared protein expression in PCa and BPH tissue biopsies using quantitative tandem mass tag (TMT) and a MultiNotch data acquisition proteomic on an Orbitrap Fusion. Four proteins that were observed to be differentially abundant in the mass spectrometry analysis were selected for further comparison with quantitative real-time PCR: S100A4, L-lactate dehydrogenase B-chain (LDHB), Phosphatidylethanolamine-binding-protein 1-RAF (RKIP), and Ras suppressor-protein-1 (RSU1). Mass spectrometry showed RKIP and RSU1 to be upregulated in PCa, while S100A4 and LDHB were upregulated in BPH. q-PCR results were in agreement with quantitative proteomic data in BPH tissue but disagree with gene expression analysis of PCa samples. These four elements showed higher gene expression in BPH than in PCa. Taken together, our results complement and reinforce the current understanding of prostate cancer progression.

Specific expression pattern of tissue cytokines analyzed through the Surface Acoustic Wave technique is associated with age-related spontaneous benign prostatic hyperplasia in rats

The aim of the study reported herein was to evaluate the suitability of the Surface Acoustic Wave (SAW) technique as a possible diagnostic tool in benign prostatic hyperplasia (BPH). Moreover, for the first time, the BPH model was a totally physiological using naturally aged rats with spontaneous, age-related BPH instead of the pharmacologically induced models usually used. Eighteen male Wistar rats were distributed according to their age: 6 weeks (young), 12 weeks (adult) and 12 months (old) old. Prostate gland was removed and analyzed by mini-arrays, Western blotting (WB) and SAW techniques. Mini-arrays indicated that there were significant differences in the expression of 29/34 inflammation-related cytokines. WB was carried out to confirm the results after selection of 4 cytokines from which one showed no changes, namely PDGF-AA, and the other three, which significantly increase in older animals, were CD86, β-NGF and VEGF. Notwithstanding, WB of old rats yielded confusing results due to an anomalous migration of proteins, dismissing this technique as an useful tool in these animals. Accurate results in old rats were uniquely obtained by using the SAW technique. Thus, SAW analysis showed that there were not differences among groups in the amount of PDGF-AA. On the contrary, SAW analysis showed that amounts of CD86, β-NGF and VEGF in old rats were 2.0, 1.9 and 5.7-fold higher than that from young ones, respectively. These results indicate that SAW is a highly accurate technique for determining changes in the cytokines expression in BPH.

AgNOR histochemical expression in benign prostatic hyperplasia and prostatic adenocarcinoma

Benign prostatic hyperplasia and prostatic adenocarcinoma were common diseases and usually occurred after the 5th decade of life. The problem in diagnosing using Hematoxylin and Eosin staining was how to differentiate whether it is benign or malignant zone. Therefore, proliferating markers, such as AgNOR, could be helping to over this difficulty. A descriptive study using consecutive sampling as the method of sample recruiting was conducted to describe AgNOR histochemical expression in benign prostatic hyperplasia and prostatic adenocarcinoma. AgNOR staining was done in 13 benign prostatic hyperplasia samples and 7 prostatic adenocarcinoma samples, which have been confirmed using p63 immunohistochemical staining before. Benign prostatic hyperplasia usually showed lower AgNOR proliferating activity while all of theprostatic adenocarcinoma (100%) had high AgNOR proliferating activity.

Prostatic Carcinogenesis: More Insights.

Background:Prostatic carcinoma ranks as the second most common malignant tumor and the fifth cause of cancer-related deaths in men. Many studies now focus on the different molecules involved in prostatic carcinogenesis. Maspin and prohibitin (PHB) are suggested to play crucial roles in the development and progression of many cancers; however, their roles in prostatic carcinogenesis have not been fully elucidated.Aim:This work was designed to study the immunohistochemical expression of maspin and PHB in prostatic carcinoma in comparison to their expression in benign prostatic hyperplasia (BPH) to give more insights about their roles in prostatic carcinogenesis.Materials and Methods:Archival blocks of 30 cases of prostatic adenocarcinomas and 15 cases of BPH were subjected to histopathological examination and immunohistochemical evaluation of maspin and PHB expression.Results:Maspin showed higher expression in prostatic carcinoma (88.9% of cases) compared to BPH (20% of cases). PHB expression was detected only in prostatic carcinoma (84.4% of cases), while all cases of BPH were negative. The expression of both maspin and PHB showed statistically significant increase with increasing Gleason score (P = 0.0125 and 0.0065 respectively).Conclusions:Overexpression of maspin and PHB in prostatic carcinoma reflects their vital roles in prostatic carcinogenesis. Their upregulation with increasing Gleason score indicates their prognostic significance. Moreover, PHB may differentiate between prostatic carcinoma and BPH being expressed only by malignant cells.

Bax-interacting factor-1 inhibits cell proliferation and promotes apoptosis in prostate cancer cells.

Prostate cancer (PCa) is one of the most common malignant tumors and the second leading cause of cancer-related death among males. Bax-interacting factor-1 (Bif-1) is a member of Endophilin family, which binds to and activates the BAX protein in response to the apoptosis signaling pathway. Loss of Bif-1 may suppress the intrinsic pathway of apoptosis and promote tumorigenesis, but there is also converse evidence that Bif-1 could in part be responsible for the tumorigenesis and the role of Bif-1 in PCa development is not clear. In the present study, we aimed to understand the relationships between Bif-1 expression and PCa development. The mRNA and protein expression levels of Bif-1 in PCa cell lines, benign prostatic hyperplasia (BPH) (n=100) and PCa tissues (n=100, including low Gleason-scored PCa n=43 and high Gleason-scored PCa n=57) were detected and the effects of Bif-1 overexpression on the apoptosis, proliferation and migration in LNCaP cells were explored. Bif-1 mRNA levels of PCa cell lines were analyzed by real-time PCR and the protein levels were detected by western blotting. Bif-1 expression in BPH and PCa samples was detected by immunohistochemistry. To build Bif-1 overexpression PCa cells, Bif-1 gene was transfected into LNCaP cells by pcDNA3.1(+)‑Bif-1 vector. Cell apoptosis was detected by flow cytometric analysis, cell proliferation measured by 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide (MTT) assay and cell migration was analyzed by wound‑healing assay. The results proved that Bif-1 is downregulated in both PCa cell lines (P<0.01) and clinical samples (P<0.05), and Bif-1 expression is suppressed with the cancer progression (BPH vs. PCa P<0.01, and low Gleason-scored PCa vs. high Gleason-scored PCa P<0.05). Overexpression of Bif-1 could significantly inhibit cell proliferation (P<0.05) and enhancing PCa cell apoptosis (P<0.05), but it did not affect the migration ability (P>0.05). Our findings give strong evidence that Bif-1 is involved in PCa tumorigenesis and acts as a suppressor in PCa progression, and may have significance in understanding the process of PCa development.

Examination of CK2α and NF-κB p65 expression in human benign prostatic hyperplasia and prostate cancer tissues.

Protein kinase CK2 plays a critical role in cell growth, proliferation, and suppression of cell death. CK2 is overexpressed, especially in the nuclear compartment, in the majority of cancers, including prostate cancer (PCa). CK2-mediated activation of transcription factor nuclear factor kappa B (NF-κB) p65 is a key step in cellular proliferation, resulting in translocation of NF-κB p65 from the cytoplasm to the nucleus. As CK2 expression and activity are also elevated in benign prostatic hyperplasia (BPH), we sought to increase the knowledge of CK2 function in benign and malignant prostate by examination of the relationships between nuclear CK2 and nuclear NF-κB p65 protein expression. The expression level and localization of CK2α and NF-κB p65 proteins in PCa and BPH tissue specimens was determined. Nuclear CK2α and NF-κB p65 protein levels are significantly higher in PCa compared with BPH, and these proteins are positively correlated with each other in both diseases. Nuclear NF-κB p65 levels correlated with Ki-67 or with cytoplasmic NF-κB p65 expression in BPH, but not in PCa. The findings provide information that combined analysis of CK2α and NF-κB p65 expression in prostate specimens relates to the disease status. Increased nuclear NF-κB p65 expression levels in PCa specifically related to nuclear CK2α levels, indicating a possible CK2-dependent relationship in malignancy. In contrast, nuclear NF-κB p65 protein levels related to both Ki-67 and cytoplasmic NF-κB p65 levels exclusively in BPH, suggesting a potential separate impact for NF-κB p65 function in proliferation for benign disease as opposed to malignant disease.

Fatty acid synthase and hepsin expression in benign prostatic hyperplasia and prostatic carcinoma

Fatty acid synthase and hepsin expression in benign prostatic hyperplasia and prostatic carcinoma

Role of androgen receptor in prostatic neoplasia versus hyperplasia.

Androgens play a fundamental role in the growth, differentiation, and maintenance of prostate tissue. The objective of the study was to evaluate and compare the androgen receptor (AR) expression in benign prostatic hyperplasia (BPH), prostatic intraepithelial neoplasia (PIN), and prostatic adenocarcinoma. A relationship between the Gleason score and AR expression was also determined in cases of prostatic adenocarcinoma. A total of 25 cases were collected which included 10 cases of prostatic adenocarcinoma, 10 cases of BPH, and five cases of PIN. Histopathological evaluation was done to determine the type of lesion including Gleason scoring. Immunohistochemistry (IHC) was performed for AR using monoclonal anti-AR antibody. Specific AR immunostaining was present in all 25 cases in varying intensity. The staining was more intense in cases of adenocarcinoma and PIN as compared BPH. There was no significant statistical difference in the intensity of staining of AR. The Gleason score was inversely related to the intensity of AR staining in adenocarcinoma. There was no significant statistical association between the AR expression and tumor, necrosis, metastasis (TNM) stage. AR nuclear expression is present in benign and malignant prostatic epithelium. In this study, cases of prostate cancer demonstrated a higher staining intensity for AR when compared with BPH. The intensity of AR staining in prostate cancer significantly reduces as the Gleason grade of the tumor increases. The staining intensity for AR was heterogeneous specifically in cases of prostate cancer. Our results indicate that AR maybe considered as a prognostic marker in prostate cancer.

ALDH1A1 as a Cancer Stem Cell Marker: Value of Immunohistochemical Expression in Benign Prostatic Hyperplasia, Prostatic Intraepithelial Neoplasia, and Prostatic Adenocarcinoma

ALDH1A1 as a Cancer Stem Cell Marker: Value of Immunohistochemical Expression in Benign Prostatic Hyperplasia, Prostatic Intraepithelial Neoplasia, and Prostatic Adenocarcinoma

AMACR versus COX-2 expression in benign prostatic hyperplasia and prostatic adenocarcinoma

AMACR versus COX-2 expression in benign prostatic hyperplasia and prostatic adenocarcinoma

The Differential Expression and Function of the Inflammatory Chemokine Receptor CXCR5 in Benign Prostatic Hyperplasia and Prostate Cancer.

Background: Chemokine and chemokine receptors could have played an important role in tumor angiogenesis and distant metastasis. The mechanism of inflammation, expression and function of chemokines and chemokine receptors in benign prostatic hyperplasia (BPH) and prostate cancer (PCa) remain unclear. The purpose of present study is to detect differential expression and function of chemokines and chemokine receptors (CCRs) in BPH and PCa.Methods: BPH-1 and peripheral blood mononuclear cells (PBMCs) were co-cultured in Transwell chambers, and human normal prostate (NP) tissues, BPH tissues and PCa tissues were collected. CCR gene-chips were used to analyze and compare the differential expression of CCRs in BPH-1 cells, BPH-1 cells co-cultured with PBMCs, and LNCaP cells. The differential expression of CCRs was detected and validated using real-time PCR, western blotting and immunofluorescence (IF). The proliferation of LNCaP cells was also investigated after the knockdown CXCR5.Results: Results of gene-chips indicated that there was low or no expression of CCR10, CXCR1, CXCR3 and CXCR5 in BPH-1 cells, whereas the expression of these receptors in BPH-1 cells was increased by PBMCs, and the expression was high in LNCaP cells. Furthermore, real-time PCR and western blotting confirmed the above mentioned results. IF verified no or low expression of CXCR1, CXCR3 and CXCR5 in NP tissues, low or moderate expression in BPH and high expression in PCa. However, CCR10 was not expressed at detectable levels in the three groups. The growth and proliferation of LNCaP cells was markedly inhibited after down-regulation of CXCR5.Conclusions: PCa cells expressed high levels of CCR10, CXCR1, CXCR3 and CXCR5. Although BPH cells did not express these factors, their expression was up-regulated when BPH-1 cells were incubated with inflammatory cells. Finally, down-regulation of CXCR5 inhibited the growth and proliferation of LNCaP cells.