DAPK Promoter Methylation and Bladder Cancer Risk: A Systematic Review and Meta-Analysis

Dai, Lihe; Ma, Chao; Zhang, Zhensheng; Zeng, Shuxiong; Liu, Anwei; Tang, Shijie; Ren, Qian; Sun, Yinghao; Xu, Chuanliang

doi:10.1371/journal.pone.0167228

Cited by 20 publications

(24 citation statements)

References 45 publications

(46 reference statements)

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“…Hypermethylation of gene promoter is a known epigenetic strategy to silence apoptogenic genes by different types of cancers as a way to allow cancer cells to propagate. In this aspect, DAPK1 is methylated at CpG islands in several tumors, which can be used as a biomarker for cancer detection and management . Pharmacological hypomethylation of DAPK1 gene with 5‐AZA‐2′‐deoxycytidine (5‐AZA‐CdR) resulted in the restoration of DAPK1's antitumor functions and acted as anticancer agent .…”

Section: Dapks Cellular Functionsmentioning

confidence: 99%

Death‐associated protein kinase (DAPK) family modulators: Current and future therapeutic outcomes

Farag

Roh

2018

Medicinal Research Reviews

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Serine/threonine kinases (STKs) represent the majority of discovered kinases to date even though a few Food and Drug Administration approved STKs inhibitors are reported. The third millennium came with the discovery of an important group of STKs that reshaped our understanding of several biological signaling pathways. This family was named death-associated protein kinase family (DAPK family). DAPKs comprise five members (DAPK1, DAPK2, DAPK3, DRAK1, and DRAK2) and belong to the calcium/calmodulin-dependent kinases domain. As time goes on, the list of biological functions of this family is constantly updated. The most extensively studied member is DAPK1 (based on the publications number and Protein Data Bank reported crystal structures) that plays fundamental biological roles depending on the cellular context. DAPK1 regulates apoptosis, autophagy, contributes to the pathogenesis of Alzheimer's disease, acts as a tumor suppressor, inhibits metastasis, mediates the body responses to viral infections, and regulates the synaptic plasticity and depression. For their biological roles, several DAPKs' modulators have been reported for treatment of many diseases as well as acting as probe compounds to facilitate the understanding of the biological functions elicited by this family. Despite that, the number of reported modulators is still limited and more research needs to be conducted on the discovery of novel strategies to activate or inhibit this family. In this report, we aim at drawing more attention to this family by reviewing the recent updates regarding the structure, biological roles, and regulation of this family. In addition, the small-molecule modulators of this family are reviewed in details with their potential therapeutic outcomes evaluated to help medicinal chemists develop more potent and selective possible drug candidates.

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Section: Dapks Cellular Functionsmentioning

confidence: 99%

Death‐associated protein kinase (DAPK) family modulators: Current and future therapeutic outcomes

Farag

Roh

2018

Medicinal Research Reviews

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“…Methylation of tumor suppressor gene promoter leads to transcription inactivation and is involved in tumorigenesis [14]. DAPK gene is closely associated with cancer genesis by inducing the suppression of cell proliferation and the product of DAPK gene is considered to be a positive mediator of apoptosis [18,19].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, evidence supported that ultrasonography may be one of the follow-up substitutes for cystoscopy in low risk UBC [13]. Furthermore, a previous study also pointed out that UBC patients had significant increased DAPK promoter methylation than those in normal controls, suggesting DAPK promoter methylation could serve as a biomarker for UBC detection [14]. Although, UBC diagnosis is mainly depended on cystoscopy and urinary cytology, nevertheless both test have certain drawbacks and the existing limitations of cytology and cystoscopy have fostered the research on alternative, minimally invasive, approaches for UBC diagnosis.…”

Section: Introductionmentioning

confidence: 90%

Combination role of DAPK methylation in urinary sediment and B ultrasound in evaluating follow-up of urinary bladder cancer

Wang

Jiang

et al. 2020

Preprint

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Background: Urinary bladder cancer (UBC) is a highly prevalent disease and is associated with substantial morbidity, mortality and cost. This paper aims to explore the combination role of DAPK methylation in urinary sediment and B ultrasound in diagnosing recurrent UBC. Methods: A total of 1021 cases of primary UBC undergone electrocision of bladder tumor through urethra were included and were subjected to follow up every 3 month within 2 years. B ultrasound, DAPK methylation in urinary sediment, examination of exfoliated cells in urine and cystoscopy were performed during the follow up. The data recorded in follow up were subjected to chi-square test and Kappa test. ROC was drawn to evaluate the diagnostic role of each parameter in recurrent UBC. Results: Among the 1021 patients, 115 patients were found with recurrent UBC by cystoscopy and biopsy two years after the operation, and failed to complete the follow up, thus the effective number of follow up was 906. The cystoscopy results were not only consistent with that of B ultrasound (Kappa = 0.785, P < 0.05), but also agreed with that of DAPK methylation in urinary sediment and combination of B ultrasound with DAPK methylation (Kappa = 0.517, P < 0.05, Kappa = 0.593, P < 0.05). ROC curve indicated that the area under curve of combination of B ultrasound with DAPK methylation was 0.922 (sensitivity, 92.86%; specificity, 91.63%; Youden index, 0.845) with negative prediction value of 99.4% which suggested that the recurrent risk would be low in case negative results were obtained.Conclusion: Those data supported that combination of DAPK methylation with B ultrasound has high performance in diagnosing recurrent UBC.

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“…The NOS quality scores ranged from 0 to 9 stars, and article scores with 6 or more stars were considered to be qualified. 15 …”

Section: Methodsmentioning

confidence: 99%

Association Between the Asp312Asn, Lys751Gln, and Arg156Arg Polymorphisms inXPDand the Risk of Prostate Cancer

Xiao

Zhang

et al. 2017

Technol Cancer Res Treat

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Prostate cancer is the most common solid cancer and genetic factors play important roles in its pathogenesis. XPD is one of the 8 core genes involved in the nucleotide excision repair pathway. The relationship between Asp312Asn, Lys751Gln, and Arg156Arg polymorphisms in XPD and prostate cancer risk is a controversial topic. Therefore, we conducted a meta-analysis to explore the relationship between these 3 polymorphisms and the risk of developing prostate cancer. We searched the electronic literature in PubMed and Google Scholar for all relevant studies (last updated January 1, 2017). The pooled odds ratios and 95% confidence intervals for the associations between the Asp312Asn, Lys751Gln, or Arg156Arg polymorphisms in XPD and prostate cancer risk were calculated. To evaluate the effects of specific study characteristics on the association of these 3 polymorphisms and prostate cancer risk, we performed subgroup analysis if 2 or more studies were available. After an extensive literature review, 7 publications regarding Asp312Asn genotype distribution with 8 case–controls, 9 publications regarding Lys751Gln genotype distribution with 10 case–controls, and 3 publications regarding Arg156Arg genotype distribution with 4 case–controls were selected. The results showed that Asp312Asn (odds ratio = 1.34, 95% confidence interval: 0.96-1.87, P = .000), Lys751Gln (odds ratio = 0.98, 95% confidence interval: 0.89-1.08, P = .986), and Arg156Arg (odds ratio = 1.05, 95% confidence interval: 0.91-1.22, P = .57) polymorphisms do not increase the risk of prostate cancer in the dominant model. Further, in the subgroup analysis by ethnicity, no relationships were observed between Lys751Gln and Arg156Arg polymorphisms and prostate cancer risk. However, stratified analysis by ethnicity revealed that Asp312Asn affects African (odds ratio = 1.57, 95% confidence interval: 1.06-2.33, P = .382) and Asian populations (odds ratio = 2.09, 95% confidence interval: 1.39-3.14, P = .396) in homozygote comparison. In conclusion, this meta-analysis suggests that there is no general association between the Asp312Asn, Lys751Gln, and Arg156Arg polymorphisms in XPD and prostate cancer susceptibility.

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DAPK Promoter Methylation and Bladder Cancer Risk: A Systematic Review and Meta-Analysis

Cited by 20 publications

References 45 publications

Death‐associated protein kinase (DAPK) family modulators: Current and future therapeutic outcomes

Death‐associated protein kinase (DAPK) family modulators: Current and future therapeutic outcomes

Combination role of DAPK methylation in urinary sediment and B ultrasound in evaluating follow-up of urinary bladder cancer

Association Between the Asp312Asn, Lys751Gln, and Arg156Arg Polymorphisms inXPDand the Risk of Prostate Cancer

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