Risk factors for prostate cancer: A multifactorial case-control study

Malik, Saima Shakil; Batool, Rakshanda; Masood, Nosheen; Yasmin, Azra

doi:10.1016/j.currproblcancer.2018.01.014

Cited by 32 publications

(17 citation statements)

References 22 publications

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“…3 The pathogenesis of PCa involves multiple factors, including genetics and environment. 4 In addition, methylation also participates in both the etiology and pathogenesis of PCa. 5 The research of protein methylation mainly focuses on lysine and arginine residues because they play different roles in essential cellular processes.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: MCM3AP-AS1 KD Inhibits Proliferation, Invasion, and Migration of PCa Cells via DNMT1/DNMT3 (A/B) Methylation-Mediated Upregulation of NPY1R

Li¹,

Lv²,

Liu³

2020

Molecular Therapy - Nucleic Acids

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Prostate cancer (PCa) is a heterogeneous tumor that commonly occurs among males worldwide. This study explored the potential role that long non-coding RNA MCM3AP antisense RNA 1 (MCM3AP-AS1) plays in PCa progression, and investigated its mechanism. MCM3AP-AS1 and neuropeptide Y receptor Y1 (NPY1R) expression was determined in PCa cells. The regulatory role of MCM3AP-AS1 in PCa cells was defined using scratch test, Transwell assay, 5-ethynyl-2 0 -deoxyuridine (EdU) assay, and flow cytometry. Methylation-specific PCR (MSP) was used to test the methylation level of NPY1R. Subsequently, the interaction among MCM3AP-AS1, DNA methyltransferase (DNMT)1/DNMT3 (A/B), and NPY1R was investigated using RNA immunoprecipitation, RNA pull-down, and chromatin immunoprecipitation. Finally, we observed xenograft tumor in nude mice. MCM3AP-AS1 was highly, whereas NPY1R was poorly, expressed in PCa. Lentivirus-mediated overexpression of MCM3AP-AS1 promoted proliferation, invasion, and migration while suppressing apoptosis of PCa cells, whereas opposite trends were detected after inhibition of the mitogenactivated protein kinase (MAPK) pathway. MCM3AP-AS1 promoted methylation of NPY1R promoter via recruitment of DNMT1/DNMT3 (A/B), thereby downregulating NPY1R expression to activate the MAPK pathway. Furthermore, overexpressed MCM3AP-AS1 was observed to facilitate PCa development in vivo, which could be reversed by overexpressed NPY1R. Altogether, MCM3AP-AS1 silencing inhibits PCa progression by disrupting methylation of the NPY1R promoter to inactivate the MAPK pathway.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: MCM3AP-AS1 KD Inhibits Proliferation, Invasion, and Migration of PCa Cells via DNMT1/DNMT3 (A/B) Methylation-Mediated Upregulation of NPY1R

Li¹,

Lv²,

Liu³

2020

Molecular Therapy - Nucleic Acids

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“… 4 PCa incidence rates also increase with age. 40 We reported crude incidence rates which show what is actually happening when there is no adjustment for age. Across the study time period, the crude incidence rates were generally highest in the three Maritime provinces of Prince Edward Island, New Brunswick and Nova Scotia.…”

Section: Discussionmentioning

confidence: 99%

Socioeconomic Gradients in Prostate Cancer Incidence Among Canadian Males: A Trend Analysis From 1992 to 2010

et al. 2021

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Introduction Understanding the effects of socioeconomic status on cancer incidence and their trends over time will help inform public health interventions for cancer control. This study sought to investigate trends in socioeconomic inequalities in prostate cancer incidence among Canadian males. Methods Using a census division level dataset (n = 280) constructed from the Canadian Cancer Registry, Canadian Census of Population (1992, 1996, 2001, 2006) and 2011 National Household Survey, we examined the effect of socioeconomic status on prostate cancer incidence among Canadian males between 1992 and 2010. The age-adjusted concentration index was used to quantify education/income-related inequalities in prostate cancer incidence. Results The crude prostate cancer incidence increased from 115 to 137 per 100 000 males in Canada from 1992 to 2010 with a peak in 2007. The rate increased significantly in all but three of four western provinces. The age-adjusted concentration index showed a higher concentration of prostate cancer diagnoses among males living in high-income neighbourhoods in Canada in particular from 1996 to 2005. In contrast, the index was higher among males living in less-educated neighbourhoods in the most recent study years (2006–2010). Conclusions The concentration of new prostate cancer cases among high-income populations in Canada may be explained by the rise of opportunistic screening of asymptomatic males; however, this should be studied in further detail. Since we found a higher incidence rate of prostate cancer among less-educated males in Canada in recent years, risk-benefit investigation of primary prevention and opportunistic screening for less-educated males is advised.

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“…Higher the specificity of the association between a factor and its effect, the more precise the relationship between a factor and its effect. PC is a multifactorial disease 46 . Together with HPV, the role of other non-infectious factors and oncogenic viruses (EBV and John Cunningham virus) in PC development is also well studied worldwide 42,47 .…”

Section: Resultsmentioning

confidence: 99%

Identification of correlation between human papillomavirus and prostate cancer: Bradford Hill Criteria Based Evaluation.

Usman¹,

Ahmad

Hameed

et al. 2021

Int. j. endorsing health sci. res.

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Background: Human papillomavirus (HPV) association has effectively been decoded in prostate cancer (PC) worldwide with controverting conclusions. Though the different groups of researchers explored the potential association of HPV with PC using meta-analysis but it still remains controversial due to the major limitations. Therefore, the present study was designed to investigate the potential link of HPV with PC using Bradford Hill criteria. Methodology: Initially using PubMed, we extracted studies that associated HPV to PC. Then, to assess the potential association of HPV with PC, an examination of the available data on HPV in PC, normal/benign samples was conducted using all the major Bradford Hill criteria postulates. Furthermore, to improve the authenticity of the present study, we have also critically evaluated the methodologies of the identified studies to check the possibility of false-negative and false-positive results. Results: After a careful assessment of the previous studies against Bradford Hill criteria postulates, we observed that all the major postulates were not fulfilled, including strength, temporality, consistency, plausibility, biological gradient, experiment, specificity, and analogy. Conclusion: The findings of this systematic review suggest no casual association of HPV with PC.

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Risk factors for prostate cancer: A multifactorial case-control study

Cited by 32 publications

References 22 publications

RETRACTED: MCM3AP-AS1 KD Inhibits Proliferation, Invasion, and Migration of PCa Cells via DNMT1/DNMT3 (A/B) Methylation-Mediated Upregulation of NPY1R

RETRACTED: MCM3AP-AS1 KD Inhibits Proliferation, Invasion, and Migration of PCa Cells via DNMT1/DNMT3 (A/B) Methylation-Mediated Upregulation of NPY1R

Socioeconomic Gradients in Prostate Cancer Incidence Among Canadian Males: A Trend Analysis From 1992 to 2010

Identification of correlation between human papillomavirus and prostate cancer: Bradford Hill Criteria Based Evaluation.

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