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Table of Contents
EDITORIAL
Year : 2019  |  Volume : 30  |  Issue : 5  |  Page : 197-198

Adiponectin and proto-oncogene MYC in prostate cancer: How far are we with the evidence?


Department of Urology, Faculty of Medicine at Airlangga University, Dr. Soetomo Hospital, Surabaya, Indonesia

Date of Submission22-Sep-2019
Date of Web Publication24-Oct-2019

Correspondence Address:
Lukman Hakim
Department of Urology, Faculty of Medicine at Airlangga University/Dr. Soetomo Hospital, Mayjend Moestopo 6-8, Surabaya 60286
Indonesia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/UROS.UROS_69_19

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How to cite this article:
Hakim L. Adiponectin and proto-oncogene MYC in prostate cancer: How far are we with the evidence?. Urol Sci 2019;30:197-8

How to cite this URL:
Hakim L. Adiponectin and proto-oncogene MYC in prostate cancer: How far are we with the evidence?. Urol Sci [serial online] 2019 [cited 2019 Nov 22];30:197-8. Available from: http://www.e-urol-sci.com/text.asp?2019/30/5/197/269889



The GLOBOCAN data 2018 shows that prostate cancer (PCa) is the most common malignancy among males, and represents the 5th leading death of cancer in men.[1] Although some risk factors have been identified, the clear etiology of this disease remains unclear.

Obesity, adiposity, and high body mass index have found to be associated with PCa and its biochemical recurrence, but the underlying mechanism remains unknown.[2],[3] Adipocyte is a secretory organ that produces several hormones, cytokines, and growth factors called adipokines. Among these adipokines, adiponectin (APN) has been robustly studied and found to be associated with PCa.[4],[5],[6]

Studies on the association between APN and PCa have resulted in contradictory results. Some studies have proven its association, whereas others failed.[7],[8] Among those who succeeded, some confirmed positive correlations, whereas others have negatively reported.[9],[10],[11] One of the rational explanations behind these conflicted evidence was proven to be correlated with the genetic polymorphisms, leading to various risks associated with PCa. The AdipoQ rs2241766 allele and AdipoR1 rs10920531 were associated with higher risk of PCa; meanwhile, the AdipoR1 rs2232853 variant was associated with a lower risk.[12]

The current predominance of evidence has shown an inverse correlation between APN and prostate malignancy. Therefore, an alteration of APN may potentially be used as a marker for early detection, to predict metastasis and a guidance for targeted therapy.[13]

Moreover, the proto-oncogene MYC is a family of regulator genes that code for transcription factors. It consists of c-MYC (also refers to MYC), I-MYC, and n-MYC. The proto-oncogene MYC has been thought to be responsible for the regulation of cellular metabolism, proliferation, and apoptosis. Its amplification occurs in 10%–30% of localized PCa, and more than 50% of advanced tumors have been linked to poorer prognosis.[14],[15],[16],[17]

Studies on MYC as a biomarker for PCa have been intensively conducted, mainly using immunohistochemistry technique to identify the expression of MYC and correlate them with the clinicopathological aspects of PCa. Various MYC antibodies, cellular staining localization (nucleus or cytoplasmic), and scoring systems have been adopted, leading to various conclusions related to PCa.[18] A study by Pettersson et al. (2018) on MYC at the protein and mRNA level has shown that neither MYC protein overexpression nor MYC mRNA overexpression is a strong prognostic marker following radical prostatectomy.[17] Some studies have reported a positive association between MYC expression and clinicopathological factors of PCa, whereas others have negatively reported or even proven to be unassociated.[19],[20],[21] The short half-life of MYC protein, the different role between MYC protein and MYC gene amplification, and the possibility of different gene amplification rather than 8q/8q24 are all the possible explanations to these contradictory evidence.

Looking back to the current evidence of APN and proto-oncogene MYC in their relation to the clinicopathological factors of PCa, further studies need to be conducted focusing on the exact association, prior to its application in the clinical setting.



 
  References Top

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Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 2018;68:394-424.  Back to cited text no. 1
    
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Hu MB, Liu SH, Jiang HW, Bai PD, Ding Q. Obesity affects the biopsy-mediated detection of prostate cancer, particularly high-grade prostate cancer: A dose-response meta-analysis of 29,464 patients. PLoS One 2014;9:e106677.  Back to cited text no. 2
    
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Bai PD, Hu MB, Xu H, Zhu WH, Hu JM, Yang T, et al. Body mass index is associated with higher Gleason score and biochemical recurrence risk following radical prostatectomy in Chinese men: A retrospective cohort study and meta-analysis. World J Surg Oncol 2015;13:311.  Back to cited text no. 3
    
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Ikeda A, Nakagawa T, Kawai K, Onozawa M, Hayashi T, Matsushita Y, et al. Serum adiponectin concentration in 2,939 Japanese men undergoing screening for prostate cancer. Prostate Int 2015;3:87-92.  Back to cited text no. 9
    
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Rider JR, Fiorentino M, Kelly R, Gerke T, Jordahl K, Sinnott JA, et al. Tumor expression of adiponectin receptor 2 and lethal prostate cancer. Carcinogenesis 2015;36:639-47.  Back to cited text no. 11
    
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Hu MB, Xu H, Hu JM, Zhu WH, Yang T, Jiang HW, et al. Genetic polymorphisms in leptin, adiponectin and their receptors affect risk and aggressiveness of prostate cancer: Evidence from a meta-analysis and pooled-review. Oncotarget 2016;7:81049-61.  Back to cited text no. 12
    
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Tumminia A, Vinciguerra F, Parisi M, Graziano M, Sciacca L, Baratta R, et al. Adipose tissue, obesity and adiponectin: Role in endocrine cancer risk. Int J Mol Sci 2019;20. pii: E2863.  Back to cited text no. 13
    
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Zafarana G, Ishkanian AS, Malloff CA, Locke JA, Sykes J, Thoms J, et al. Copy number alterations of c-MYC and PTEN are prognostic factors for relapse after prostate cancer radiotherapy. Cancer 2012;118:4053-62.  Back to cited text no. 14
    
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Qian J, Hirasawa K, Bostwick DG, Bergstralh EJ, Slezak JM, Anderl KL, et al. Loss of p53 and c-myc overrepresentation in stage T(2-3)N(1-3)M(0) prostate cancer are potential markers for cancer progression. Mod Pathol 2002;15:35-44.  Back to cited text no. 15
    
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Bivalacqua TJ, Kendirci M, Champion HC, Hellstrom WJ, Andersson KE, Hedlund P. Dysregulation of cGMP-dependent protein kinase 1 (PKG-1) impairs erectile function in diabetic rats: Influence ofin vivo gene therapy of PKG1alpha. BJU Int 2007;99:1488-94.  Back to cited text no. 16
    
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Pettersson A, Gerke T, Penney KL, Lis RT, Stack EC, Pértega-Gomes N, et al. MYC overexpression at the protein and mRNA level and cancer outcomes among men treated with radical prostatectomy for prostate cancer. Cancer Epidemiol Biomarkers Prev 2018;27:201-7.  Back to cited text no. 17
    
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Koh CM, Bieberich CJ, Dang CV, Nelson WG, Yegnasubramanian S, De Marzo AM. MYC and prostate cancer. Genes Cancer 2010;1:617-28.  Back to cited text no. 18
    
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Fromont G, Godet J, Peyret A, Irani J, Celhay O, Rozet F, et al. 8q24 amplification is associated with Myc expression and prostate cancer progression and is an independent predictor of recurrence after radical prostatectomy. Hum Pathol 2013;44:1617-23.  Back to cited text no. 19
    
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Prowatke I, Devens F, Benner A, Gröne EF, Mertens D, Gröne HJ, et al. Expression analysis of imbalanced genes in prostate carcinoma using tissue microarrays. Br J Cancer 2007;96:82-8.  Back to cited text no. 20
    
21.
Gurel B, Iwata T, Koh C, Jenkins RB, Lan F, Van Dang C, et al. Nuclear MYC protein overexpression is an early alteration in human prostate carcinogenesis. Mod Pathol 2008;21:1156-67.  Back to cited text no. 21
    




 

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