DigitalUM :: Browsing by Subject "Prostate cancer"

Browsing by Subject "Prostate cancer"

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Anogenital distance, a biomarker of prenatal androgen exposure Is associated with prostate cancer severity
(Wiley, 2016-11-16) Maldonado-Cárceles, Ana B.; Sánchez-Rodríguez, Carlos; Vera-Porras, Eva M.; Oñate-Celdrán, Julián; Samper Mateo, Paula; García Escudero, Damián; Torres-Roca, Marcos; Martínez Díaz, Francisco; Mendiola, Jaime; Torres Cantero, Alberto Manuel; Arense Gonzalo, Julián Jesús; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica
BACKGROUND. Anogenital distance (AGD), the distance from the centre of the anus to the genitals, is a sexually dimorphic phenotype in mammals. Experimental studies have shown that AGD is a biomarker of prenatal androgen exposure during the masculinisation period of development. The aim of this study is to assess the relationship between anogenital distance (AGD), as an indirect marker of prenatal hormonal environment, and prostate cancer (PCa) severity. MATERIALS. We conducted a cross-sectional study with a total of 120 PCa patients with confirmed biopsy of the tumour from April 2007 to July 2015. Two variants of the anogenital distance were assessed, from the anus to the posterior base of the scrotum (AGDAS) and to the cephalad insertion of the penis (AGDAP). We compared differences in groups to evaluate the association between AGD measurements and severity of the preoperative biopsy and clinical scores. RESULTS. Longer AGDAS was significantly associated with the highest Gleason score (P = 0.015) and D'Amico nomogram (P = 0.048). In contrast, no statistical differences were found in the AGDAP and severity of the preoperative biopsy. CONCLUSIONS. These findings are consistent with the hypothesis that a higher prenatal androgen exposure is associated with higher severity of PCa. Prostate.
Open Access
Anticancer properties of carotenoids in prostate cancer. A review
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) da Costa Pereira Soares, Nathalia; Junger Teodoro, Anderson; Falagan Lotsch, Priscila; Mauro Granjeiro, José; Borojevic, Radovan
Prostate cancer is the most common noncutaneous cancer of men in the world. Several epidemiological studies have linked increased carotenoids consumption with decreased prostate cancer risk. These findings are supported by in vitro and in vivo experiments showing that carotenoids not only enhance the antioxidant response of prostate cells, but that they are able to inhibit proliferation, induce apoptosis and decrease the metastatic capacity of prostate cancer cells. However, clear clinical evidence supporting the use of carotenoids in prevention or treatment of prostate cancer is not available, due to the limited number of published randomized clinical trials, and the varying protocols used in the existing studies. The scope of the present review is to discuss the potential impact of carotenoids on prostate cancer by giving an overview of the molecular mechanisms and in vitro / in vivo effects.
Open Access
Bone morphogenetic proteins and their receptor signaling in prostate cancer
(Murcia : F. Hernández, 2007) Ye, L.; Lewis-Russell, J.M.; Kynaston, H.G.; Jiang, W.G.
Bone morphogenetic proteins (BMPs) belong to the TGF-ß superfamily and are vital bone inductive factors. BMPs also play important roles during embryonic development and the postnatal homeostasis of various organs and tissues, by controlling cellular differentiation, proliferation and apoptosis. Prostate cancer is the most common cancer in men in Western countries, with a high incidence of bone metastasis. Once bony metastasis developed, the condition is incurable, and contributes significant disease specific morbidity and mortality. However, the mechanisms underlying the development of bone metastasis remain unclear. BMPs have been implicated in the development of both primary and secondary tumors, particularly skeletal metastasis. Aberrations in BMPs signaling have also been identified in various neoplasms. Recently studies have also suggested a pivotal role in bone metastasis for Noggin, which is a BMP antagonist. In this review, we discuss the current knowledge of BMPs signaling, abnormalities which have been identified and their involvement in tumour progression, and particularly in the development of bone metastasis in prostate cancer.
Open Access
Cáncer de próstata: conocimientos e interferencias enla promoción y prevención de la enfermedad
(Murcia: Servicio de Publicaciones de la Universidad de Murcia, 2019) Oliveira, Pâmela Scarlatt Durães; Miranda, Sérgio Vinicius Cardoso de; Barbosa, Henrique Andrade; Rocha, Rodrigo Marques Batista da; Rodrigues, Adriana Barbosa; Silva, Vanessa Maia da
El artículo objetivó describir la percepción de los hombres sobre el cáncer de próstata y los factores de prevención relacionados. Se trata de un estudio cualitativo del tipo de ensayo comunitario. Se realizaron tres reuniones en forma de grupo focal, compuesto por 60 hombres con rango de edad superior a 40 años, abordando el tema del cáncer de próstata. Para el análisis de los datos cualitativos se realizó el análisis de contenido temático y los datos fueron organizados en el software -Atlas Ti. Los resultadosfueron referenciados en los objetivos de este estudio y enfatizados en categorías. Los datos evidenciaron que todavía hay una barrera física y social a ser superada ante los estigmas masculinos, y existe una carencia de conocimiento sobre la prevención de este cáncer. El aumento de la oferta de exámenes diagnósticos, agilidad en la atención, horarios diferenciados para los trabajadores son algunas de las estrategias eficientes para atraer a esta población para la prevención del cáncer de próstata.
Open Access
Cancer-associated fibroblast-secreted exosomes promote prostate cancer cell migration and invasion by the FGL1/SOX5 axis
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Kong, Lingquan; Wang, Xing; Li, Yu; Zhang, Xiansheng
Exosomes secreted by cancer-associated fibroblasts (CAFs) play a critical role in cancer progression. This study aimed to explore the effects of CAF exosomes on prostate cancer (PC) cell metastasis. PC cells were treated with these exosomes, and their processes were evaluated using cell-counting kit-8 and Transwell assays. Exosome-regulated mRNAs were explored using quantitative real-time PCR. The relationship between FGL1 and SOX5 was analyzed using co-immunoprecipitation and fluorescence in situ hybridization (FISH) assays. The results of this study showed that exosomes derived from CAFs promoted PC cell viability, migration, and invasion. CAFs promoted PC cell viability and metastasis by releasing exosomes. Exosome treatment increased the levels of FGL1, which interacted with SOX5 and negatively regulated its expression. Rescue experiments demonstrated that CAF exosomes promoted the biological behaviors of PC cells by upregulating FGL1 and downregulating SOX5. Moreover, exosomes accelerated tumor growth by regulating the FGL1 level. In conclusion, CAF-derived exosomes promoted PC cell viability, migration, and invasion by elevating the FGL1/SOX5 axis, suggesting a novel strategy for the treatment of metastatic PC.
Open Access
CD63 is a diagnostic marker of prostate cancer and a prognostic marker of biochemical progression following radical prostatectomy
(2026) Marit Bernhardt1; Isabella Federica Bollen; Tobias Kreft; Anna Katrin Scherping; Xiaolin Zhou; Manuel Ritter; Jörg Ellinger; Carsten Stephan; Glen Kristiansen; Elisabeth Dingendorf; Biología Celular e Histología
Aims. We aimed to analyze CD63, a cell surface protein that has been associated with tumor aggressiveness in several cancers, including breast, colorectal, and lung cancer, as well as melanoma, in prostate cancer. Methods. CD63 expression was analyzed immuno histochemically in a cohort of primary prostate cancers from 281 patients. The results were correlated with clinico-pathologic parameters, including biochemical recurrence. In addition, CD63 expression in 251 of the 281 patients with prostate cancer was compared with CD63 expression in matched benign tissue samples (490 tissue samples). The analysis was performed automatically using the open-source software QuPath© and tested for statistical significance. For comparison with the diagnostic markers AMACR and GOLPH2, CD63 was analyzed in an additional cohort of 198 prostate cancers. Results. CD63 expression was found in 100% of prostate cancer cases and benign tissue spots. Increased CD63 expression was significantly associated with higher tumor stage (pT), tumor grade (ISUP), as well as shorter progression-free survival (PFS). Compared with the CD63 intensity of benign tissue, expression in tumor tissue was higher in >80% of cases. In addition, combining the expression of CD63 and AMACR, positivity reached 97.2%, making CD63 a promising diagnostic biomarker in challenging cases. Conclusions. CD63 is commonly overexpressed in prostate cancer, and higher levels are associated with earlier biochemical tumor progression; hence, CD63 is a promising diagnostic and prognostic biomarker in primary prostate cancer.
Open Access
Cell proliferation and apoptosis in prostate cancer. significance in disease progression and therapy
(Murcia : F. Hernández, 2000) Kyprianou, N.; Bruckheimer, E.M.; Guo, Y.
Recent biochemical and genetic studies have substantially increased our understanding of death signal transduction pathways, making it clear however, that apoptosis is not a single-lane, one-way street. Rather, multiple parallel pathways have been identified. For instance, analysis of bcl-2, bax, p53, and caspase knockout mice while establishing distinct roles for each of these apoptotic players, they also provided valuable information for the design of specific inhibitors of apoptosis. Thus blocking one pathway, as in caspase knockout mice, what we observe is not a complete suppression of apoptosis but rather a delay in apoptosis induction (Hakem et al., 1998; Kuida et al., 1998). In view of nature's means of ensuring activation of a compensatory apoptotic response, when one pathway fails in developing prostate cancer therapeutic interventions, the challenge remains to further dissect individual apoptotic pathways. Advances in our understanding of the integrated functions governing prostate cell proliferation and cell death, clearly suggest that effective prostate cancer therapies are not only molecularly targeted, but that are also customized to take into account the delicate balance of opposing growth influences in the ageing gland. In this review we discuss the evidence on the significance of molecular deregulation of the key players of this growth equlibrium, apoptosis and cell proliferation in prostate cancer progression, and the clinical implications of changes in the apoptotic response in disease detection and therapy.
Open Access
Dendritic and lymphocytic cell infiltration in prostate carcinoma
(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Yishan, Liu; Thorstein, Sæter; Vlatkovic, Ljiljana; Servoll, Einar; Waaler, Gudmund; Axcrona, Ulrika; Giercksky, Karl- Erik; Nesland, Jahn M.; Zhen-He, Suo; Axcrona, Karol
We examined the distribution of CD1a+ cells and CD8+ and CD4+ T lymphocytes in prostate cancer (PCa) and correlated these with clinicopathological parameters. We also investigated whether the distribution of these cells was related to the expression of the cell membrane protein B7-H3, a putative negative regulator of the immune response expressed on PCa cells. A cohort of 151 PCa patients treated with radical prostatectomy (RP) was followed prospectively from 1985 until 2006 with a median follow-up of 9 years. Whole-mount sections of PCa specimens were immunostained to identify immune cells. A low number of CD1a+ cells was significantly associated with a high Gleason score and high pathological stage of pT3. The number of CD1a+ cells correlated significantly with the number of intratumoral and stromal CD8+ and stromal CD4+ lymphocytes. Kaplan-Meier analysis showed a tendency toward impaired biochemical progression-free survival in patients with few CD1a+ cells within their RP specimens. The expression of B7-H3 correlated inversely with the number of CD1a+ cells and intratumoral CD4+ lymphocytes; there was a trend for a similar inverse relationship between B7-H3 expression and the number of CD8+ lymphocytes. Our findings suggest that high-grade prostate carcinoma cells manipulate the immune system and that these changes contribute to the mechanism underlying tumor escape from immune surveillance.
Open Access
Diagnostic and prognostic value of T-cell receptor gamma alternative reading frame protein (TARP) expression in prostate cancer
(Murcia: F. Hernández, 2010) Fritzsche, Florian R.; Stephan, Carsten; Gerhardt, Josefine; Lein, Michael; Hofmann, Irina; Jung, Klaus; Dietel, Manfred; Kristiansen, Glen
T-cell receptor gamma chain alternative reading frame protein (TARP) has recently been proposed as being up-regulated in prostate cancer (PCA). Additionally, TARP has been proposed as a potential therapeutic target for cancer therapy. We analysed the protein expression of TARP in a large well characterised prostate cancer cohort to assess its diagnostic and prognostic value. Methodologically, we constructed a tissue microarray comprising more than 600 PCA cases including matching benign prostate tissue. TARP protein expression was carefully analysed and associated with clinico-pathological parameters, PSA-relapse free survival and expression data of established and proposed diagnostic markers (AMACR, p63, GOLPH2). Our results show that TARP is significantly over-expressed in the vast majority (~85%) of PCA in comparison to non neoplastic prostate tissue. Its expression was associated with conventional markers of unfavourable and more aggressive tumour behaviour. However, a prognostic value of TARP could not be found. The diagnostic value of TARP is limited in comparison to AMACR, p63 or GOLPH2. Since TARP specific immunologic therapy regimen are currently being tested, the high frequency of TARP overexpression in PCA conveys a high potential for a predictive and potentially therapeutic use of this biomarker.
Open Access
Downregulation of miR-485-3p promotes proliferation, migration and invasion in prostate cancer through activation of TGF-β signaling
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Chen, Dongdong Chen; Fan, Jiaxing; Li, Xianduo; Jiao, Zongshuai; Tang, Guanbao; Guo, Xuewen; Chen, Hao; Wang, Jianning; Men, Tongyi
Background. Prostate cancer (PC) is the second leading cause of cancer-related death among men worldwide. Downregulation of miR-485-3p has been revealed to participate in the tumorigenesis and progression of many types of cancer. However, the clinical and biological role of miR-485-3p in PC remains largely unknown. Methods. The expression of miR-485-3p was analyzed in the published databases and detected in our clinical samples and cell lines by RT-qPCR assay. CCK8, transwell invasion and migration, and colony formation assays were performed to investigate the biological function of miR-485-3p. Bioinformatical analysis, RIP, western blotting and luciferase reporter assays were carried out to explore the downstream mechanism of miR-485-3p. Results. The level of miR-485-3p was downregulated in PC tissues, particularly in primary PC tissues with metastasis relative to normal prostate tissues. miR-485-3p downregulation was positively correlated with poor disease-free and overall survival in patients with PC. Functionally, miR-485-3p overexpression dramatically suppressed the proliferation, migration and invasion ability of PC cells in vitro. Mechanistically, miR-485-3p overexpression suppressed the activity of TGF-β signaling by targeting TGFBR2 to play tumor-suppressive roles in PC progression. Conclusion. Our study reports the miR-485- 3p/TGFBR2/ TGF-β signaling axis in tumor development of PC, suggesting miR-485-3p may be a potential target to develop therapeutic strategies against PC.
Open Access
Elucidating the role of PRMTs in prostate cancer using open access databases and a patient cohort dataset
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Grypari, Ioanna Maria; Pappa, Ioanna; Papastergiou, Thomas; Zolota, Vassiliki; Bravou, Vasiliki; Melachrinou, Maria; Megalooikonomou, Vasileios; Tzelepi, Vasiliki
Protein arginine methylation is an understudied epigenetic mechanism catalyzed by enzymes known as Protein Methyltransferases of Arginine (PRMTs), while the opposite reaction is performed by Jumonji domain- containing protein 6 (JMJD6). There is increasing evidence that PRMTs are deregulated in prostate cancer (PCa). In this study, the expression of two PRMT members, PRMT2 and PRMT7 as well as JMJD6, a demethylase, was analyzed in PCa. Initially, we retrieved data from The Cancer Genome Atlas (TCGA) project and the Gene Expression Omnibus (GEO) database to explore the differential expression of various PRMT family members in patients with PCa and then applied immunohistochemistry in a patient cohort across the spectrum of PCa, including non-neoplastic prostate tissue and lymph node metastatic foci. The results from the TCGA analysis revealed that PRMT7, PRMT6 and PRMT3 expression increased while PRMT2, PRMT9 and JMJD6 levels decreased in the tumor compared to non-neoplastic prostate. Results from the GEO datasets were similar, albeit not identical with the TCGA results, with PRMT7 and PRMT3 being upregulated and PRMT2 and JMJD6 being downregulated in the tumor compared to non-neoplastic tissue in some of them. In addition, PRMT7 levels decreased with stage and grade progression in the TCGA analysis. In the patient cohort, both PRMTs and JMJD6 were overexpressed in PCa compared to non-neoplastic tissue, and nuclear PRMT2 and JMJD6 were upregulated in lymph node metastasis, too. PRMT7 and JMJD6 expression were upregulated with the progression of stage and JMJD6 was also increased with the elevation of grade. After androgen ablation therapy, nuclear expression of PRMT7 and JMJD6 were elevated compared to untreated tumors. PRMT2, PRMT7 and JMD6 were also correlated with markers of EMT and cell cycle regulators. Finally, our findings indicate that PRMTs and JMJD6 are involved in prostate cancer progression and revealed a potential interplay of PRMTs with EMT mediators, underscoring the need for therapeutic targeting of arginine methylation in prostate cancer.
Open Access
Etoposide sensitivity of human prostatic cancer cell lines PC-3, DU 145 and LNCaP
(Murcia : F. Hernández, 1999) Salido, M.; Larran, J.; Lopez, A.; Vilches, J.; Aparicio, J.
Metastatic prostatic cancer is typically refractory to androgen ablation therapy due to the presence of androgen-independent clones in the neoplasia. A therapeutical approach which could effectively control androgen-dependent and independent cells is, thus, needed. Maybe the failure of certain cancer cells to engage in apoptosis could explain the inherent drug resistance of many tumors. Anyway, these cells can retain the ability to undergo apoptosis in response to an adequate stimulus. We tested whether etoposide, a topoisomerase I1 inhibitor, could induce apoptosis in androgen-dependent (LNCaP) as well as independent (PC-3 and DU 145) human prostate cancer cell lines. Morphological examination was performed, as it is regarded as one of the most reliable parameters for the detection of apoptotic changes. Complementarily, biochemical and flow cytometric studies were also used. Characteristical changes of apoptosis were demonstrated in PC-3, Du 145, and LNCaP cancer cells after treatment with etoposide. These cells, thus, retain the ability to undergo apoptosis under adequate conditions, in a promising approach to hormone refractory prostate cancer therapy.
Open Access
Fibroblast activation protein-alpha knockdown suppresses prostate cancer cell invasion and proliferation
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) An, Jiali; Hou, Dingkun; Wang, Lei; Wang, Lili; Yang, Yuanyuan; Wang, Haitao
Background. Prostate cancer is one of the most common malignant tumors of the male genitourinary system. Fibroblast activation protein alpha (FAP-α) overexpression has been shown to occur in a wide range of tumors. However, the specific mechanism of FAP-α in the development of prostate cancer has not been reported. Methods. In this study, real-time quantitative PCR (qRT-PCR) was used to detect the relative expression of FAP-α mRNA in prostate cancer cell lines (PC-3, LNCaP, and DU145) and human normal prostate epithelial cell line RWPE-1. Small interfering RNA (siRNA) targeting FAP-α and vectors expressing exogenous FAP-α were transfected to prostate cancer cells (LNCaP and DU145) to investigate the function of FAP-α. BALB/c nude mice were injected with DU145 cells which were transfected with NC-siRNA, FAP-αsiRNA-1, or FAP-α-siRNA-2. Results. Compared to adjacent normal tissues, FAPα protein and mRNA levels in prostate cancer tissues increased significantly (P<0.05). Compared to patients with high FAP-α mRNA levels, patients with low FAP-α mRNA levels had a significantly higher survival rate (χ2=5.050, log-rank P=0.025). Overexpression of FAP-α in LNCaP cells markedly inhibited cell apoptosis, and promoted cell invasion and proliferation. In contrast, knockdown of FAP-α expression in DU145 cells can significantly reduce invasion, proliferation, and promote apoptosis in prostate cancer. Immunofluorescence assay further indicated that down-regulation of FAP-α could suppress the nuclear translocation of β-catenin. An in vivo study found that compared with the NC-siRNA group, the tumor weight and tumor volume in the FAPα-siRNA-1 and FAP-α-siRNA-2 groups were significantly decreased. Conclusions. In conclusion, down-regulation of FAP-α can inhibit the invasion and proliferation of prostate cancer. Our study provides a theoretical basis for the targeted treatment of prostate cancer.
Open Access
Grading of the prostate carcinoma, cyto-histological correlations on 100 cases
(Murcia : F. Hernández, 1986) Dalla Palma, P.; Dante, S.; Costantin, G; Rebuffi, A.; Zattoni, F.; Plazza, R.
From January 1980 to December 1983, 154 patients underwent prostatic FNAB and histological control. The sensitivity of cytology was 85070, the specificity 68% and the predictive value of positive cases 83%. The cyto-histological correlation of the grading of the 100 prostatic carcinomas histologically confirmed (85 cytologically positive for carcinoma and 15 negative or uncertain) showed a predictive value of positive results of 58%, ranging from 42% for G3, 50% for G1 and 69% for G2. The usefulness of cytological grading is stressed to monitor the follow-up of those patients treated for prostatic carcinoma who, because of the advanced stage or age, were not surgically treated. Key words: Prostate cancer - FNAB - Cytohistological grading correlation
Open Access
Hepatocyte growth factor/scatter factor and prostate cancer: a review
(Murcia : F. Hernández, 2005) Hurle, R.A.; Davies, Graham; Parr, C.; Mason, M.D.; Jenkins, S.A.; Kynaston, H.G.; Jiang, W.G.
Men who die from prostate cancer do so from uncontrolled metastatic disease. A better understanding of the mechanisms involved in the progression and metastasis of prostate cancer may lead to novel therapeutic approaches to prevent its natural progression. Hepatocyte Growth Factor / Scatter factor (HGF/SF) has been demonstrated to elicit a number of key functions in numerous tissues that are important in the progression, invasion and metastasis of cancer. Studies have demonstrated that the activity of HGF/SF and its receptor c-Met are linked to disease progression in numerous cancers. However, research into these functions, which include activities as a mitogen, a motogen and an anti-apoptotic and angiogenic factor in prostate cancer are limited. This article reviews the published evidence of the roles HGF/SF plays in prostate cancer progression and highlights the clinical and therapeutic potential of research into this pleiomorphic cytokine.
Open Access
Hsa_circ_0070440 mediates the prognosis and progress of human prostate cancer
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Huang, Min; Zhang, Junming; Luo, Wentao; Li, Tingting; Song, Qiong; Zhang, Lixiao; Cao, Min; Li, Shuang
Background. This study was designed to explore whether hsa_circ_0070440 was dysregulated in prostate cancer (PCa), and assess the effects of hsa_circ_0070440 alteration on PCa prognosis and cell function. Methods. The expression levels of hsa_circ_ 0070440 were assessed in PCa tissues and cell lines. After the classification of patients with PCa based on mean hsa_circ_0070440 level in 138 cases, Chi-square test and survival analyses (Kaplan-Meier method and multivariable Cox proportional hazards analysis) were performed to assess the predictive value of hsa_circ_0070440 in treatment failure (TTF), time to PSA progression (TTPP) and overall survival time. To examine the function of hsa_circ_0070440 in PCa cells, 22Rv1 and C4-2B cells were used for CCK-8 proliferation and Transwell migration assays. Hsa_circ_0070440- and TXNDC5-specific bindings with miR-382/383-5p were validated by bioinformatic analysis and luciferase gene reporter assay. Results. An increased expression of hsa_circ_ 0070440 was found in PCA tissues and cell lines, associated with clinical T stage (p=0.021) and lymph node metastasis. Hsa_circ_0070440 predicted poor overall survival, TTPP, and TTF, acting as independent prognostic factors for overall survival, TTPP, and TTF in patients with PCa. Knockdown of hsa_circ_0070440 inhibited cell proliferation and migration in vitro. Furthermore, hsa_circ_0070440 could sponge miR-382/383-5p. TXNDC5 was a common target gene for miR-382/383-5p in PCa cells. Conclusion. This study demonstrated that hsa_circ_0070440 can predict the prognosis of PCa patients. Hsa_circ_0070440 can facilitate the proliferation and migration of PCa cells, possibly by sponging miR-382/383-5p
Open Access
Insight into the heterogeneity of prostate cancer through PSA-PSMA prostate clones: mechanisms and consequences
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Jemaa, Awatef Ben; Bouraoui, Yosra; Oueslati, Ridha
A major clinical challenge is posed by the current inability to readily distinguish indolent from aggressive tumors in prostate cancer patients. Research efforts are dedicated to overcome this problem by understanding the molecular basis of the transition from normal, benign cells to prostatic intraepithelial neoplasia (PIN), localized carcinoma, and metastatic cancer. Combined with the evidence of the phenotypic heterogeneity of benign prostate hyperplasia, primary tumors and metastases, it is conceivable that several prostate clones emerge progressively during tumor progression. We have identified several PSA-PSMA prostate clones during prostate cancer progression. In this paper we focus on the susceptibilities of these PSAPSMA prostate clones to factors that promote prostate hyperplastic, neoplastic and metastatic development and their consequences in disease outcome.
Open Access
Intervenciones hacia la Prueba de Antígeno Prostático: Una revisión rápida de literatura
(Universidad de Murcia. Servicio de publicaciones, 2023) Orozco Alonzo, Alfredo; Báez Hernández, Francisco Javier; Nava Navarro, Vianet; Zenteno López, Miguel Ángel; Morales Nieto, Arelia; Álvarez Blanco, Víctor Manuel
Objetivo: Identificar la mejor evidencia disponible relacionada a las intervenciones dirigidas hacia la aceptación de la prueba de antígeno prostático. Metodología:Revisión rápida de literatura, siguiendo los pasos establecidos por Tapia-Benavente, los cuales son: 1.- pregunta de investigación, para lo cual se utilizó la estructura PICO acotada a la definición del problema, intervención y resultado; 2.- búsqueda de bibliografía en bases de datos reconocidas; 3.- selección de estudios y extracción de datos; 4.- evaluación del riesgo de sesgo, para lo cual se utilizó la guía de comprobación de ensayos clínicos del grupo CONSORT; y 5.- la elaboración de la síntesis además de la conclusión de la evidencia encontrada. Resultados: La búsqueda rápida de literatura arrojó un total de 51 publicaciones de tres bases de datos, PubMed (27), EBSCO (13) y SCOPUS (11); de los cuales 11 cumplían con los criterios de inclusión. El 100% de los estudios indican un cambio significativo entre el grupo experimental y control (p < .05). Las estrategias más utilizadas incluyen la visita domiciliaria, conferencias, debates en grupo, lluvia de ideas, dinámicas de pregunta y respuesta con diapositivas, así como presentación de folletos educativos, mismos que se ejecutan en un periodo de un día, hasta seis meses. Conclusiones: Se hace evidente el vacío de conocimiento referente al desarrollo e implementación de estrategias para abordar la conducta de prevención relacionada al Cáncer de Próstata hacia varones de pueblos originarios, así como la falta de modelos de intervención de enfermería enfocadas en este padecimiento.
Open Access
LncRNA UBE2R2-AS1, as prognostic marker, promotes cell proliferation and EMT in prostate cancer
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Wang, Feng; Zhao, Miao; Jiang, Yuehong; Xia, Silong; Sun, Dapeng; Zhou, Dahong; Dong, Zipu
Background. Long noncoding RNA ubiquitin-conjugating enzyme E2 R2 antisense RNA 1 (UBE2R2-AS1) has been recently reported to participate in the progression of tumors, including glioma and liver cancer. However, the roles of UBE2R2-AS1 in prostate cancer (PC) remained poorly understood. Methods. The expression of UBE2R2-AS1 was determined in tumor tissues and paired adjacent tissues from PC patients using quantitative reverse transcription PCR analysis. Correlation between UBE2R2-AS1 expression and clinicopathological parameters and overall survival were investigated by Chi-square test and Kaplan-Meier method analysis. The in vitro experiments, including CCK-8 assay, colony formation, flow cytometry and transwell assay were performed to investigate the functional role of UBE2R2-AS1 knockdown or overexpression on PC cell lines (PC-3 and DU145). Related protein expression levels were measured by western blot analysis. Results. Our data showed that UBE2R2-AS1 expression was significantly upregulated in PC tissues compared with that in adjacent tissues. The high levels of UBE2R2-AS1 were associated with high Gleason score, advanced clinical T stage, lymph node metastasis and poor prognosis. Knockdown of UBE2R2-AS1 suppressed cell proliferation, migration and invasion, induced cell cycle G0/G1 arrest and apoptosis in PC cells, along with decreased expression of PCNA, CDK4, Cyclin D1, Bcl-2, N-cadherin and Vimentin, and increased E-cadherin expression. Overexpression of UBE12R2-AS1 obtained the opposite results in PC cells. Conclusions. Our findings suggest that UBE2R2- AS1 might be a potential diagnostic and/or therapeutic target in PC.
Open Access
Molecular therapeutics in prostate cancer
(Murcia : F. Hernández, 2003) Nicholson, B.; Theodorescu, D.
The purpose of this review is to provide information on the molecular basis of prostate cancer biology and to identify some of the targets for therapy, and highlight some potential strategies for molecular treatment. Here we give a synopsis of what we have learned regarding molecular biology of cancer in general and the directions research might take in the future in order to impact prostate cancer specifically. This work is certainly not encyclopedic in nature and we apologize in advance to colleagues whose work we were no able to include. Hope lies in learning to utilize some of these molecular workings for better prevention, diagnosis, and treatment of the most common solid organ cancer in men. Prostate cancer is a formidable disease and at current rates of diagnosis will affect one-in-six men living in the United States (Greenlee et al., 2000) Many of these men are diagnosed at an early stage of the disease and can be effectively treated by surgery or radiation. However, a significant fraction of men are diagnosed with later stage disease or progress despite early curative therapeutic attempts. Unfortunately, many of these men succumb to prostate cancer, as management options are limited and not always successful. Through an understanding of the molecular processes that occur in the development and progression of prostate cancer, novel therapies will arise that will provide longer survival, better quality of life, and a chance for cure in men afflicted with this disease.