Knowledge and Awareness of Prostate Cancer Among the General Public in Burkina Faso

The lack of awareness about prostate cancer and other prostate-related issues has been identified as a cause of low survival and higher mortality rates among black men. The aim of this study is to assess the knowledge of prostate cancer (PCa) among men in the general public, in the main city of Burkina Faso (Ouagadougou). The targeted population was black African men aged 25 years and older, with no history of PCa. Six hundred men who provided informed consent were invited to participate in a PCa knowledge questionnaire through face-to-face interviews. The questionnaire was composed of multiple-choice items designed to ascertain participant’s characteristics (age, profession, and level of education) and knowledge of prostate and PCa (risk factors, diagnosis tests, and curative treatments). The average age of men was 42 (min 25, max 80), and 63 % reported primary school or less. Sixty-two percent admitted they did not know the terms prostate and prostate cancer. Only two respondents (0.3 %) cited race as a risk factor, when 90 (15 %) perceived too much sexual activity as a risk factor. A majority of respondents (70.3 %, n?=?422) stated that they were unaware of any diagnosis tests for PCa. The level of education was strongly correlated with PCa knowledge (p?<?0.001). Men in the city of Ouagadougou have poor knowledge of PCa. Educational interventions should target the entire populations to improve self-informed decision about early diagnostic possibilities of PCa.     

A pilot study of prostate cancer knowledge among African American men and their health care advocates: implications for screening decisions

Purpose

Prostate cancer (PCa) is the second leading cause of cancer death in U.S. men [American Cancer Society (ACS)], most often affecting men age 50 and older. The study provides information about factors that influence rural AA men in their decision to undergo screening for PCa with a specific focus on PCa knowledge among AA men and their health care advocates.

Methods

A longitudinal quantitative study included AA males and their health care advocates. Participants were from three Alabama rural counties. Measures included demographics, PCa knowledge, decisional conflict, and health literacy scales.

Results

Thirty-three men with a mean age of 54.61 and 35 health care advocates were included in the study. PROCASE Knowledge Index measure results indicate a lack of PCa knowledge among both male primary participants and their advocates. The knowledge of AA men in the study was somewhat low, with individuals correctly answering approximately six questions out of ten at multiple time points (baseline total M?=?6.42, SD?=?1.52). Decisional conflict responses at 12 months (38.64) were lower than at baseline (M?=?62.88) and at 6 months (M?=?58.33), p?<?.005.

Conclusion

Health care advocates of the 33 male participants were usually women, spouses, or significant others, supporting the vital role women play in men’s health specifically in rural underserved communities. Low overall PCa knowledge, including their risk for PCa, among these participants indicates a need for PCa and screening educational interventions and dialogue that include males and their significant others.

     

Impact of undergoing prostate carcinoma screening on prostate carcinoma-related knowledge and distress

BACKGROUND: Despite the ongoing controversy regarding the utility of prostate carcinoma (PCa) screening, the prevalence of asymptomatic men who participate in free PCa screening programs is on the rise. However, this increased awareness has not been associated with increased knowledge about the potential limitations of PCa creening. We conducted a prospective assessment to delineate men's motivations for undergoing screening and to determine the impact of screening on psychological distress and on men's knowledge about PCa screening. METHODS: We conducted two telephone interviews with a group of 136 men registered to undergo free PCa screening at two hospital-based sites. The first interview was conducted before screening and the second interview followed receipt of the screening results. Interviews assessed demographics and screening history, reasons for undergoing the current screening, cancer-related and general psychological distress, knowledge of risk factors for PCa, and knowledge of the benefits and limitations of screening. Only participants with normal screening results were included in these analyses. RESULTS: "Seeking peace of mind about prostate cancer" was rated as the most important reason for undergoing screening. PCa-related distress decreased following receipt of a negative result (P < 0.01). Stratified analyses indicated that this was particularly true among younger men and African American men (both Ps < 0.001). Awareness of the benefits of screening was very high, but awareness of limitations was low, with fewer limitations reported following screening compared with prescreening (P < 0.01). Although awareness of the established risk factors improved following screening, controversial risk factors (i.e., those with limited empirical support) and factors that were unrelated to PCa risk were also rated as more important in the development of PCa than they were before screening (all Ps < 0.05). Therefore, the results may reflect that following screening, participants were simply more likely to endorse plausible risk factors, rather than actually reflecting an increase in participants' knowledge. CONCLUSIONS: These results suggest the importance of developing informed consent procedures and educational programs for the asymptomatic men who participate in free prostate screening programs each year, as the decision to be screened is being made without the benefit of a full understanding of the current state of medical knowledge about PCa screening. Until the definitive results of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial are available, improved patient education is needed to assist men in making screening decisions consistent with their own preferences.     

Urologists’ and GPs’ knowledge of hereditary prostate cancer is suboptimal for prostate cancer counseling: a nation-wide survey in The Netherlands

A family history of prostate cancer (PCa) is an established risk factor for PCa. In case of a positive family history, the balance between positive and adverse effects of prostate-specific antigen (PSA) testing might be different from the general population, for which the European Randomized Study of Screening for Prostate Cancer (ERSPC) showed a beneficial effect on mortality. This, however, went at the cost of considerable overtreatment. This study assessed Dutch physicians' knowledge of heredity and PCa and their 'post-ERSPC' attitude towards PCa testing, including consideration of family history. In January 2010, all Dutch urologists and clinical geneticists (CGs) and 300 general practitioners (GPs) were invited by email to complete an anonymous online survey, which contained questions about hereditary PCa and their attitudes towards PCa case-finding and screening. 109 urologists (31%), 69 GPs (23%) and 46 CGs (31%) completed the survey. CGs had the most accurate knowledge of hereditary PCa. All but 1 CG mentioned at least one inherited trait with PCa, compared to only 25% of urologists and 9% of GPs. CGs hardly ever counseled men about PCa testing. Most urologists and GPs discuss possible risks and benefits before testing for PCa with PSA. Remarkably, 35-40% of them do not take family history into consideration. Knowledge of urologists and GPs about heredity and PCa is suboptimal. Hence, PCa counseling might not be optimal for men with a positive family history. Multidisciplinary guidelines on this topic should be developed to optimize personalized counseling.     

miRNAs as biomarkers in prostate cancer

Current prostate cancer (PCa) diagnosis is based in the serum prostate-specific antigen biomarker and digital rectal examination. However, these methods are limited by a low predictive value (24?C37?%) and a high risk of mistaken results. During last years, new promising biomarkers such as Prostate Cancer Antigen 3 (PCA-3) and TMPRSS2-ETS fusion genes have been evaluated for their clinical use. However, the search of new biomarkers that could be used for PCa diagnosis and prognosis is still needed. Recent studies have demonstrated that the aberrant expression of microRNAs (miRNAs), small non-coding RNAs that negatively regulate gene expression, is related with the development of several cancers, including PCa. Since miRNAs serve as phenotypic signatures of different cancers, they appear as potential diagnostic, prognostic and therapeutic tools. Here, we review the current knowledge of miRNA expression patterns in PCa and their role in PCa prognosis and therapeutics.     

Informed decision making on PSA testing for the detection of prostate cancer: An evaluation of a leaflet with risk indicator

BackgroundPopulation-based screening for prostate cancer (PCa) remains controversial. To help men making informed decisions about prostate specific antigen (PSA) screening a risk indicator (www.uroweb.org) was developed. This risk indicator is embedded in a leaflet that informs men about the pros and cons of PCa screening and enables calculation of the individual risk of having a biopsy detectable PCa.AimTo assess the effect of providing a leaflet including individualized risk estimation on informed decision making of men, i.e. knowledge about PCa and PSA screening, attitude towards undergoing a PSA test and intention to have a PSA test.MethodsAn intervention study among 2000 men, aged 55–65 years, randomly selected from the population registry of the city of Dordrecht, the Netherlands, in 2008. Men were sent a questionnaire on knowledge of PCa, attitude and intention to have a PSA test. Men without a history of (screening for) PCa were sent the leaflet and Questionnaire 2 within 2 weeks after returning Questionnaire 1. Validated health and anxiety measures were used.ResultsOne thousand and twenty seven of 2000 men completed Questionnaire 1 (51%), of whom 298 were excluded due to a history of (screening for) PCa. Of the 729 remaining men, 601 completed Questionnaire 2 as well. At the second assessment significantly more men met the requirements of informed decision making (15% versus 33%, p < 0.001), more men had relevant knowledge (284/601, 50% versus 420/601, 77%, p < 0.001) and the intention to have a PSA test had increased (p < 0.001).ConclusionsProviding information on PCa screening combined with individualized risk estimation enhanced informed decision making and may be used for shared decision making on PSA screening of physicians and patients.     

Association of Some Polymorphisms in the VDR Gene,CYP17 Gene and SRD5A2 Gene and Prostate Cancer among Lebanese Men

Aims: The goal of the study was to investigate possible association of some single nucleotide polymorphisms(SNPs) in the VDR gene (the FokI, BsmI, ApaI and TaqαI loci), and the CYP17 gene (the MspA1I locus), and 0 or 9TA repeats in the SRD5A2 gene, and prostate cancer (PCa) among Lebanese men. Materials and Methods: BloodDNA of 69 subjects with confirmed PCa and 69 controls, all about 50 years of age or older, was subjected to PCR orPCR-restriction fragment-length polymorphism (PCR-RFLP) analyses, and the risk-bearing and the protective alleleswere identified. The odds ratio (OR) of having a genotype and the relative risk (RR) of developing PCa were calculated.In addition, the distributions of homozygosis and heterozygosis in the risk-bearing alleles and the protective allelesamong the control and the PCa groups were compared. Results: The f allele of the VDR FokI locus and the (TA) 9repeat allele of the SRD5A2 gene were found to be associated with increased risks of PCa (p = 0.006 and 0.050,respectively). Homozygosis in the risk-bearing alleles was rare both in the control and the PCa groups. A higherfraction of the controls compared to the PCa group was double-homozygous in the two protective alleles (52.2% forcontrols, 24.6% for PCa group, p = <0.001). Conclusions: To the best of our knowledge, this is the first genetic studydemonstrating the association of certain polymorphisms of the VDR gene and the SDR5A2 gene and increased risk ofPCa among Lebanese men. Our study also indicates that the overall polymorphism profile of all genes involved inthe prostate physiology is likely to be a better indicator for PCa risk than the polymorphisms in the individual genes.     

Genetic susceptibility to prostate cancer: a review

A genetic component in prostate cancer has been recognized since decades. Through numerous epidemiological and molecular biological studies, much evidence has accumulated in favor of a significant but heterogeneous hereditary component in prostate cancer (PCa) susceptibility. Since the mapping of a high-penetrant PCa susceptibility locus at 1q24–25, much attention has been paid to the identification of PCa susceptibility genes. So far, seven loci have been mapped, and at three of these loci, genes have been cloned and mutations identified. Yet their role in hereditary and sporadic disease is still under debate and probably very modest. Although research on hereditary prostate cancer has improved our knowledge of the genetic etiology of the disease, still a lot of questions remain unanswered. Here, we aim to review the genetic epidemiological and molecular biological research in the field of hereditary prostate cancer and the problems that are encountered with this research.     

Immunohistochemical expression and localization of somatostatin receptor subtypes in androgen ablated prostate cancer

Objective

The aim was to examine the expression and localization of the five somatostatin receptors (termed SSTR1 to 5) in radical prostatectomies (RPs) from patients with prostatic adenocarcinoma (PCa) under complete androgen ablation (CAA) before operation.

Material

The five SSTRs were evaluated in the epithelial, smooth muscle and endothelial cells of normal-looking epithelium (Nep), high-grade prostatic intraepithelial neoplasia (HGPIN) and PCa in 20 RPs with clinically detected PCa from patients under CAA. Twenty RPs with clinically detected PCa from hormonally untreated patients were used as control group.

Results

Concerning the secretory cells (i) Membrane staining was seen for SSTR3 and SSTR4; the mean percentages of positive cells, higher in SSTR3 than in SSTR4, decreased sharply in HGPIN and PCa compared with Nep; the mean percentages in the androgen ablated group were 30% to 90% lower than in the untreated; (ii) Cytoplasmic staining was seen for all five SSTRs; the mean percentages of positive cells in Nep, HGPIN and PCa of the untreated group were similar, and in general as high as 80% or more; in the treated group, the Nep values were similar to those in the untreated, whereas the values in HGPIN and PCa were lower for SSTR1, three and five, with a decrease of 30% for SSTR1; (iii) Nuclear staining was seen with SSTR4 and SSTR5, the mean percentages for the former being much lower than for the latter; treatment affected both HGPIN and PCa, whose proportions of stained cells were 30% to 55% lower than in the untreated group. Cytoplasmic staining in the basal cells was seen for all five SSTRs, both in Nep and HGPIN. The values in the treated group were lower than in the other, the difference between the two group being in general comprised between 10% and 40%. Treatment did not affect SSTR staining in the smooth muscle and endothelial cells.

Conclusions

The present study expands our knowledge on the expression and localization of the five SSTRs in the prostate following CAA.     

Association of Vitamin D Receptor Gene Polymorphisms with Prostate Cancer Risk in the Pakistani Population

Background: Vitamin D receptor (VDR) gene has been a subject of extensive pharmacogenetic researchrecently. Association studies between different types of cancers including prostate cancer (PCa) and VDR genepolymorphism have also been conducted. The objective of this study was to find possible associations betweenPCa and VDR gene polymorphisms in the Pakistani population. Materials and Methods: A total of 162 subjects,including prostate cancer patients and controls, were genotyped for Apa I, Taq I and Fok I polymorphisms inthe VDR gene using allele specific PCR, PCR-RFLP and direct DNA sequencing. Allelic frequencies were testedfor Hardy-Weinberg equilibrium and associations between the genetic markers and PCa were calculated usinglogistic regression. Results: Apa I CC genotype was found to have strongest association with PCa risk, and “A”genotype was found to have protective effect. Fok I and Taq I did not have appreciable levels of association withPCa, although Taq I “TC” heterozygotes seemed to have some protective effect. Similarly the “C” allele of Fok Ialso seemed to have protective effect. Conclusions: To our knowledge, this is the first report showing associationbetween VDR gene polymorphisms and PCa in Pakistan. Our findings may be somewhat skewed because ofsmall sample size and tendency of consanguineous marriages in Pakistani society; nevertheless, it shows thetrend of association and protective effects of certain VDR gene polymorphisms against PCa.     

The ADAM9/UBN2/AKR1C3 axis promotes resistance to androgen-deprivation in prostate cancer

Metastatic and castration-resistant disease is a fatal manifestation of prostate cancer (PCa). The mechanism through which resistance to androgen deprivation in PCa is developed remains largely unknown. Our understanding of the tumor microenvironment (TME) and key signaling pathways between tumors and their TME is currently changing in light of the generation of new knowledge with regard to cancer progression. A disintegrin and metalloproteinase domain-containing protein 9 (ADAM9) is a membranous bridge forming cell-cell and cell-matrix connections that regulate tumor aggressiveness and metastasis. However, it is not known whether ADAM9 expressed in the TME contributes to the CRPC phenotype. In this study, we aimed to investigate the expression patterns of ADAM9 in prostate cancer-associated fibroblasts (CAFs). We also intended to elucidate the effects of both stromal cell- and cancer cell-derived ADAM9 on the progression of CRPC and the implicated molecular pathways. By using both clinical specimens and cell lines, we herein showed that unlike the membrane anchored ADAM9 overexpressed by both PCa cells and prostate CAFs, the secreted isoform of ADAM9 (sADAM9) was strongly detected in CAFs, but rarely in tumor cells, and that could be a serum marker for PCa patients. We demonstrated that functionally sADAM9 are characterized as chemoattractant for the directed movement of androgen-independent PCa cells through integrin downstream FAK/AKT pathway, supporting that elevated sADAM9 by prostate CAFs could be responsible for the promotion of CRPC metastasis. Moreover, by stimulating PCa cells with sADAM9, we found that ubinuclein-2 (UBN2) expression was increased. A positive correlation of ADAM9 and UBN2 expression was observed in androgen receptor-expressing PCa cell lines and further confirmed in clinical PCa specimens. Using a genetic modification approach, we identified UBN2 as a downstream target gene of ADAM9 that is critical for the survival of androgen-dependent PCa cells in response to androgen deprivation, through the induction and effect of the aldo-keto reductase family 1 member C3 (AKR1C3). Collectively, our results reveal a novel action of ADAM9 on the transition of androgen-dependent PCa cells into an androgen-independent manner through the UBN2/AKR1C3 axis; the aforementioned action could contribute to the clinically-observed acquired androgen-deprivation therapy resistance.     

Primary cancers before and after prostate cancer diagnosis

BACKGROUND:

The occurrence of multiple cancers may indicate common etiology; and, although some studies have investigated the risk of second primary cancers after prostate cancer (PCa), there are no studies on cancers before PCa.

METHODS:

The PCBaSe Sweden database is based on the National Prostate Cancer Register (NPCR), which covers >96% of PCa cases. The authors estimated the prevalence and cumulative incidence of different cancers before and after PCa diagnosis in 72,613 men according to PCa treatment and disease stage in PCBaSe and their matched comparison cohort of men who were free of PCa.

RESULTS:

In total, 6829 men were diagnosed with another primary cancer before their PCa diagnosis, including 138 men at the time of PCa diagnosis and 5230 men were diagnosed after PCa diagnosis. Cancer of the bladder or colon and nonmelanoma of the skin were the 3 most frequently observed cancers before and after PCa diagnosis. At the time of PCa diagnosis, the prevalence of these 3 cancers was 1.94% for bladder cancer, 1.08% for colon cancer, and 1.08% for nonmelanoma skin cancer, compared with 1.30%, 0.96%, and 1.03%, respectively, for the matched comparison cohort. Five years after PCa diagnosis, the difference in incidence proportion between PCa men and their comparison cohort was 7‰ (95% CI, 5.6‰‐8.5‰), 1.3‰ (0‰‐2.6‰), and 1.6‰ (0.6‰‐2.6‰) for these 3 cancers, respectively. From a uro‐oncologic point of view, it is interesting to note that the prevalence of kidney cancer at the time of PCa diagnosis was 0.42% compared with 0.28% for the matched comparison cohort.

CONCLUSIONS:

Approximately 17% of all PCa occurred in combination with another primary cancer (before or after PCa diagnosis). Detection bias probably explains part of this observation, but further investigations are required to assess possible underlying mechanisms. Cancer 2012. © 2012 American Cancer Society.     

Infiltrated pre-adipocytes increase prostate cancer metastasis via modulation of the miR-301a/androgen receptor (AR)/TGF-β1/Smad/MMP9 signals

High fat dietary intake may increase the risk of prostate cancer (PCa). Pre-adipocytes, one of the basic components in the tumor microenvironment (TME), are capable of differentiating into adipose tissues and play key roles to affect PCa progression. Here we found the pre-adipocytes could be recruited more easily to PCa than its surrounding normal prostate tissue. In vitro co-culture system also confirmed PCa has a better capacity than normal prostate to recruit pre-adipocytes. The consequences of recruiting more pre-adipocytes may then increase PCa cell invasion. Mechanism dissection revealed infiltrating pre-adipocytes might function through down-regulation of the androgen receptor (AR) via modulation of miR-301a, and then increase PCa cell invasion via induction of TGF-β1/Smad/MMP9 signals. The mouse model with orthotopically xenografted PCa CWR22Rv1 cells with pre-adipocytes also confirmed that infiltrating pre-adipocytes could increase PCa cell invasion via suppressing AR signaling. Together, our results reveal a new mechanism showing pre-adipocytes in the prostate TME can be recruited to PCa to increase PCa metastasis via modulation of the miR-301a/AR/TGF-β1/Smad/MMP9 signals. Targeting this newly identified signaling may help us to better inhibit PCa metastasis.     

Infiltrating T cells promote prostate cancer metastasis via modulation of FGF11→miRNA‐541→androgen receptor (AR)→MMP9 signaling

Early clinical studies suggested infiltrating T cells might be associated with poor outcomes in prostate cancer (PCa) patients. The detailed mechanisms how T cells contribute to PCa progression, however, remained unclear. Here, we found PCa cells have a better capacity to recruit more CD4(+) T cells than the surrounding normal prostate cells via secreting more chemokines‐CXCL9. The consequences of more recruited CD4(+) T cells to PCa might then lead to enhance PCa cell invasion. Mechanism dissection revealed that infiltrating CD4(+) T cells might function through the modulation of FGF11→miRNA‐541 signals to suppress PCa androgen receptor (AR) signals. The suppressed AR signals might then alter the MMP9 signals to promote the PCa cell invasion. Importantly, suppressed AR signals via AR‐siRNA or anti‐androgen Enzalutamide in PCa cells also enhanced the recruitment of T cells and the consequences of this positive feed back regulation could then enhance the PCa cell invasion. Targeting these newly identified signals via FGF11‐siRNA, miRNA‐541 inhibitor or MMP9 inhibitor all led to partially reverse the enhanced PCa cell invasion. Results from in vivo mouse models also confirmed the in vitro cell lines in co‐culture studies. Together, these results concluded that infiltrating CD4(+) T cells could promote PCa metastasis via modulation of FGF11→miRNA‐541→AR→MMP9 signaling. Targeting these newly identified signals may provide us a new potential therapeutic approach to better battle PCa metastasis.     

Use of two gene panels for prostate cancer diagnosis and patient risk stratification

Currently, no ideal prostate cancer (PCa) diagnostic or prognostic test is available due to the lack of biomarkers with high sensitivity and specificity. There is an unmet medical need to develop combinations of multiple biomarkers which may have higher accuracy in detection of PCa and stratification of aggressive and indolent cancer patients. The aim of this study was to test two biomarker gene panels in distinguishing PCa from benign prostate and high-risk, aggressive PCa from low-risk, indolent PCa, respectively. We identified a five-gene panel that can be used to distinguish PCa from benign prostate. The messenger RNA (mRNA) expression signature of the five genes was determined in 144 PCa and benign prostate specimens from prostatectomy. We showed that the five-gene panel distinguished PCa from benign prostate with sensitivity of 96.59 %, specificity of 92.86 %, and area under the curve (AUC) of 0.992 (p?<?0.0001). The five-gene panel was further validated in a 137 specimen cohort and showed sensitivity of 84.62 %, specificity of 91.84 %, and AUC of 0.942 (p?<?0.0001). To define subtypes of PCa for treatment guidance, we examined mRNA expression signature of an eight-gene panel in 87 PCa specimens from prostatectomy. The signature of the eight-gene panel was able to distinguish aggressive PCa (Gleason score >6) from indolent PCa (Gleason score ≤6) with sensitivity of 90.28 %, specificity of 80.00 %, and AUC of 0.967 (p?<?0.0001). This panel was further validated in a 158 specimen cohort and showed significant difference between aggressive PCa and indolent PCa with sensitivity of 92.57 %, specificity of 70.00 %, and AUC of 0.962 (p?<?0.0001). Our findings in assessing multiple biomarkers in combination may provide new tools to detect PCa and distinguish aggressive and indolent PCa for precision and personalized treatment. The two biomarker panels may be used in clinical settings for accurate PCa diagnosis and patient risk stratification for biomarker-guided treatment.     

Bone‐induced c‐kit expression in prostate cancer: A driver of intraosseous tumor growth

Loss of BRCA2 function stimulates prostate cancer (PCa) cell invasion and is associated with more aggressive and metastatic tumors in PCa patients. Concurrently, the receptor tyrosine kinase c‐kit is highly expressed in skeletal metastases of PCa patients and induced in PCa cells placed into the bone microenvironment in experimental models. However, the precise requirement of c‐kit for intraosseous growth of PCa and its relation to BRCA2 expression remain unexplored. Here, we show that c‐kit expression promotes migration and invasion of PCa cells. Alongside, we found that c‐kit expression in PCa cells parallels BRCA2 downregulation. Gene rescue experiments with human BRCA2 transgene in c‐kit‐transfected PCa cells resulted in reduction of c‐kit protein expression and migration and invasion, suggesting a functional significance of BRCA2 downregulation by c‐kit. The inverse association between c‐kit and BRCA2 gene expressions in PCa cells was confirmed using laser capture microdissection in experimental intraosseous tumors and bone metastases of PCa patients. Inhibition of bone‐induced c‐kit expression in PCa cells transduced with lentiviral short hairpin RNA reduced intraosseous tumor incidence and growth. Overall, our results provide evidence of a novel pathway that links bone‐induced c‐kit expression in PCa cells to BRCA2 downregulation and supports bone metastasis.     

Targeting SMYD2 inhibits prostate cancer cell growth by regulating c-Myc signaling

SMYD2 is a lysine histone methyl transferase involved in various cancers epigenetically via methylating histone H3K4, and H3K36. c-Myc is one of the major drivers of prostate cancer (PCa) initiation and progression. The roles of SMYD2 in PCa and the regulators of c-Myc activity in PCa are still under-researched. SMYD2 expression and survival outcomes in PCa cohorts were analyzed by bioinformatics analysis. SMYD2 protein levels were detected in PCa tissues by immunohistochemistry. SMYD2 knockdown cells were established to identify the effects of SMYD2 on cell growth in vitro and in vivo. GSEA and RNA sequencing were adopted to reconnoiter the signaling regulated by SMYD2 in PCa. The relationship between SMYD2 and c-Myc was examined by western blot analysis, qPCR, and immunohistochemistry. SMYD2 specific inhibitor-AZ505 was used to pharmacologically inhibit SMYD2 function in vitro and in vivo. SMYD2 expression increased in PCa tissues compared with benign prostate tissues and higher SMYD2 expression was associated with a higher risk of biochemical relapse after radical prostatectomy. SMYD2 knockdown inhibited the growth of PCa cells both in vitro and in vivo. Furthermore, high SMYD2 levels conduced to activated c-Myc signaling in PCa cells. Importantly, the pharmacological intervention of SMYD2 by AZ505 significantly repressed PCa cell growth both in vitro and in vivo. Our findings indicate that SMYD2 inhibition restrains PCa cell proliferation by regulating c-Myc signaling and provide evidence for the potential practice of SMYD2 targeting in the treatment of PCa.