Volume 10, Issue 1 (Vol.10 No.1 Apr 2021)
rbmb.net 2021, 10(1): 60-68 |
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Mohammad Ghasem Kashanizadeh 
, Fariba Rezaei Fakhrnezhad , Saeede Yavari , Homa Alizadeh , Payam Hashemim , Amir Monfaredan *
, Fariba Rezaei Fakhrnezhad , Saeede Yavari , Homa Alizadeh , Payam Hashemim , Amir Monfaredan *
Department of Hematology, Faculty of Medicine, Tabriz Branch, Islamic Azad University, Tabriz, Iran.
Abstract: (3031 Views)
Background: Prostate cancer is the second most common cancer in men in Iran. It can be treated in the early stages of the disease; therefore, early diagnosis can be lifesaving. The aim of this study was to investigate the molecular expression of some oncogenes and predisposing behaviors contributing to the aggressiveness of prostate cancer.
Methods: In this case-control study, prostate cancer specimens were collected from both patients and healthy volunteers. Several factors such as age, family history, smoking, and stage of the disease, were investigated based on the criteria of this study. Real-time PCR was used to measure the expression of four oncogenes. Statistical analysis of our data was carried out using SPSS software version 22.
Results: The X2 test showed that there was a difference in the incidence of prostate cancer in different age groups (X2= 9.30; p= 0.026). Although data analysis by the X2 test showed that family history had a significant effect on prostate cancer (X2= 14.43; p= 0.001), smoking did not show a significant effect on the incidence of this disorder (X2= 4.67; p= 0.097). The T2N1M0 stage is the most common form of prostate cancer in patients with family history of prostate cancer and the habit of smoking. Also, the expression of KRAS1P, GLB1L2, SChLAP1 and PACSIN3 oncogenes reduced in prostate cancer samples compared to the control group.
Conclusions: Overall, functional interpretation of gene expression in the prostate tissue can affect tumor progression. Yet, further practical studies are required to reveal the accurate underlying mechanisms.
Methods: In this case-control study, prostate cancer specimens were collected from both patients and healthy volunteers. Several factors such as age, family history, smoking, and stage of the disease, were investigated based on the criteria of this study. Real-time PCR was used to measure the expression of four oncogenes. Statistical analysis of our data was carried out using SPSS software version 22.
Results: The X2 test showed that there was a difference in the incidence of prostate cancer in different age groups (X2= 9.30; p= 0.026). Although data analysis by the X2 test showed that family history had a significant effect on prostate cancer (X2= 14.43; p= 0.001), smoking did not show a significant effect on the incidence of this disorder (X2= 4.67; p= 0.097). The T2N1M0 stage is the most common form of prostate cancer in patients with family history of prostate cancer and the habit of smoking. Also, the expression of KRAS1P, GLB1L2, SChLAP1 and PACSIN3 oncogenes reduced in prostate cancer samples compared to the control group.
Conclusions: Overall, functional interpretation of gene expression in the prostate tissue can affect tumor progression. Yet, further practical studies are required to reveal the accurate underlying mechanisms.
Type of Article: Original Article |
Subject:
Cell Biology
Received: 2020/09/1 | Accepted: 2020/09/14 | Published: 2021/05/9
Received: 2020/09/1 | Accepted: 2020/09/14 | Published: 2021/05/9
References
1. Jhun MA, Geybels MS, Wright JL, Kolb S, April C, Bibikova M, et al. Gene expression signature of Gleason score is associated with prostate cancer outcomes in a radical prostatectomy cohort. Oncotarget. 2017;8(26):43035-43047. [DOI:10.18632/oncotarget.17428] [PMID] [PMCID]
2. Jonsson M, Ragnum HB, Julin CH, Yeramian A, Clancy T, Frikstad K-AM, et al. Hypoxia-independent gene expression signature associated with radiosensitisation of prostate cancer cell lines by histone deacetylase inhibition. Br J Cancer. 2016;115(8):929-939. [DOI:10.1038/bjc.2016.278] [PMID] [PMCID]
3. Kazantseva M, Mehta S, Eiholzer RA, Gimenez G, Bowie S, Campbell H, et al. The Δ133p53β isoform promotes an immunosuppressive environment leading to aggressive prostate cancer. Cell Death Dis. 2019;10(9):631. [DOI:10.1038/s41419-019-1861-1] [PMID] [PMCID]
4. Caraceni A, Zecca E, Formaglio F, Ricchini F. Bone Metastases from Prostate Cancer: From Symptom Control to Pain Palliation. Bone Metastases from Prostate Cancer. 2017:251-270. [DOI:10.1007/978-3-319-42327-2_19]
5. Prensner JR, Iyer MK, Sahu A, Asangani IA, Cao Q, Patel L, et al. The long noncoding RNA SChLAP1 promotes aggressive prostate cancer and antagonizes the SWI/SNF complex. Nat Genet. 2013;45(11):1392-8. [DOI:10.1038/ng.2771] [PMID] [PMCID]
6. Ito K. Prostate cancer in Asian men. Nature Reviews Urology. 2014;11(4):197-212. [DOI:10.1038/nrurol.2014.42] [PMID]
7. Joniau S, Briganti A, Gontero P, Gandaglia G, Tosco L, Fieuws S, et al. Stratification of high-risk prostate cancer into prognostic categories: a European multi-institutional study. Eur Urol. 2015;67(1):157-164. [DOI:10.1016/j.eururo.2014.01.020] [PMID]
8. Han M, Partin AW, Zahurak M, Piantadosi S, Epstein JI, Walsh PC. Biochemical (prostate specific antigen) recurrence probability following radical prostatectomy for clinically localized prostate cancer. J Urol. 2003;169(2):517-23.
https://doi.org/10.1097/00005392-200302000-00018 [DOI:10.1016/S0022-5347(05)63946-8] [PMID]
9. Hosseinzadeh O, Hekmat Z, Nekoufar S, Ahmad M, Mohammadzadeh N, Monfaredan A. Evaluate the gene expression of TPT1, EDN3, and ANO7 in prostate cancer tissues and their relation with age, tumor stage and family history. Meta Gene. 2020;24:100671. [DOI:10.1016/j.mgene.2020.100671]
10. Santarius T, Shipley J, Brewer D, Stratton MR, Cooper CS. A census of amplified and overexpressed human cancer genes. Nature Reviews Cancer. 2010;10(1):59-64. [DOI:10.1038/nrc2771] [PMID]
11. Quinn DI, Henshall SM, Sutherland RL. Molecular markers of prostate cancer outcome. European journal of cancer. 2005;41(6):858-887. [DOI:10.1016/j.ejca.2004.12.035] [PMID]
12. Fredriksson NJ, Ny L, Nilsson JA, Larsson E. Systematic analysis of noncoding somatic mutations and gene expression alterations across 14 tumor types. Nat Genet. 2014;46(12):1258-63. [DOI:10.1038/ng.3141] [PMID]
13. Poliseno L, Salmena L, Zhang J, Carver B, Haveman WJ, Pandolfi PP. A coding-independent function of gene and pseudogene mRNAs regulates tumour biology. Nature. 2010;465(7301):1033-1038. [DOI:10.1038/nature09144] [PMID] [PMCID]
14. Silan F, Gultekin Y, Atik S, Kilinc D, Alan C, Yildiz F, et al. Combined point mutations in codon 12 and 13 of KRAS oncogene in prostate carcinomas. Mol Biol Rep. 2012;39(2):1595-9. [DOI:10.1007/s11033-011-0898-8] [PMID]
15. Mehra R, Udager AM, Ahearn TU, Cao X, Feng FY, Loda M, et al. Overexpression of the long non-coding RNA SChLAP1 independently predicts lethal prostate cancer. Eur Urol. 2016;70(4):549-552. [DOI:10.1016/j.eururo.2015.12.003] [PMID] [PMCID]
16. Roach W, Plomann M. PACSIN3 overexpression increases adipocyte glucose transport through GLUT1. Biochem Biophys Res Commun. 2007;355(3):745-50. [DOI:10.1016/j.bbrc.2007.02.025] [PMID] [PMCID]
17. Zhang L, Wang C-Y, Yang R, Shi J, Fu R, Chen L, et al. Real-time quantitative RT-PCR assay of prostate-specific antigen and prostate-specific membrane antigen in peripheral blood for detection of prostate cancer micrometastasis. Urologic Oncology: Seminars and Original Investigations. 2008:634-640. [DOI:10.1016/j.urolonc.2007.07.016] [PMID]
18. Hassanipour S, Fathalipour M, Salehiniya H. The incidence of prostate cancer in Iran: a systematic review and meta-analysis. Prostate Int. 2018;6(2):41-45. [DOI:10.1016/j.prnil.2017.11.003] [PMID] [PMCID]
19. Mousavi SM, Gouya MM, Ramazani R, Davanlou M, Hajsadeghi N, Seddighi Z. Cancer incidence and mortality in Iran. Annals of oncology. 2009;20(3):556-563. [DOI:10.1093/annonc/mdn642] [PMID]
20. Sadeghi-Gandomani H, Yousefi M, Rahimi S, Yousefi S, Karimi-Rozveh A, Hosseini S, et al. The incidence, risk factors, and knowledge about the prostate cancer through worldwide and Iran. World Cancer Research Journal. 2017;4(4):e972. [DOI:10.15419/bmrat.v4i9.371]
21. Tang B, Han CT, Gan HL, Zhang GM, Zhang CZ, Yang WY, et al. Smoking increased the risk of prostate cancer with grade group≥ 4 and intraductal carcinoma in a prospective biopsy cohort. Prostate. 2017;77(9):984-989. [DOI:10.1002/pros.23354] [PMID]
22. De Nunzio C, Tema G, Lombardo R, Trucchi A, Bellangino M, Esperto F, et al. Cigarette smoking is not associated with prostate cancer diagnosis and aggressiveness: a cross sectional Italian study. Minerva Urol Nefrol. 2018;70(6):598-605. [DOI:10.23736/S0393-2249.18.03182-X] [PMID]
23. Putra IBO, Hamid AR, Mochtar CA, Umbas R. Relationship of age, prostate-specific antigen, and prostate volume in Indonesian men with benign prostatic hyperplasia. Prostate Int. 2016;4(2):43-8. [DOI:10.1016/j.prnil.2016.03.002] [PMID] [PMCID]
24. Kurian CJ, Leader AE, Thong MS, Keith SW, Zeigler-Johnson CM. Examining relationships between age at diagnosis and health-related quality of life outcomes in prostate cancer survivors. BMC Public Health. 2018;18(1):1060. [DOI:10.1186/s12889-018-5976-6] [PMID] [PMCID]
25. Taheri M, Habibi M, Noroozi R, Rakhshan A, Sarrafzadeh S, Sayad A, et al. HOTAIR genetic variants are associated with prostate cancer and benign prostate hyperplasia in an Iranian population. Gene. 2017;613:20-24. [DOI:10.1016/j.gene.2017.02.031] [PMID]
26. Barber L, Gerke T, Markt SC, Peisch SF, Wilson KM, Ahearn T, et al. Family history of breast or prostate cancer and prostate cancer risk. Clin Cancer Res. 2018;24(23):5910-5917. [DOI:10.1158/1078-0432.CCR-18-0370] [PMID] [PMCID]
27. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011;61(2):69-90. [DOI:10.3322/caac.20107] [PMID]
28. Nodouzi V, Nowroozi M, Hashemi M, Javadi G, Mahdian R. Concurrent down-regulation of PTEN and NKX3. 1 expression in Iranian patients with prostate cancer. Int Braz J Urol. 2015;41(5):898-905. [DOI:10.1590/S1677-5538.IBJU.2014.0036] [PMID] [PMCID]
29. Luo JH, Yu YP, Cieply K, Lin F, Deflavia P, Dhir R, et al. Gene expression analysis of prostate cancers. Mol Carcinog. 2002;33(1):25-35. [DOI:10.1002/mc.10018] [PMID]
30. Rose M, Kloten V, Noetzel E, Gola L, Ehling J, Heide T, et al. ITIH5 mediates epigenetic reprogramming of breast cancer cells. Mol Cancer. 2017;16(1):44. [DOI:10.1186/s12943-017-0610-2] [PMID] [PMCID]
31. Su X, Xing J, Wang Z, Chen L, Cui M, Jiang B. microRNAs and ceRNAs: RNA networks in pathogenesis of cancer. Chin J Cancer Res. 2013;25(2):235-239.
32. Xu B, Niu X, Zhang X, Tao J, Wu D, Wang Z, et al. miR-143 decreases prostate cancer cells proliferation and migration and enhances their sensitivity to docetaxel through suppression of KRAS. Mol Cell Biochem. 2011;350(1-2):207-13. [DOI:10.1007/s11010-010-0700-6] [PMID]
33. Chua ML, Lo W, Pintilie M, Murgic J, Lalonde E, Bhandari V, et al. A prostate cancer "nimbosus": genomic instability and SChLAP1 dysregulation underpin aggression of intraductal and cribriform subpathologies. Eur Urol. 2017;72(5):665-674. [DOI:10.1016/j.eururo.2017.04.034] [PMID]
34. Gou Wf, Shen Df, Yang Xf, Zhao S, Liu Yp, Sun Hz, et al. ING5 suppresses proliferation, apoptosis, migration and invasion, and induces autophagy and differentiation of gastric cancer cells: a good marker for carcinogenesis and subsequent progression. Oncotarget. 2015;6(23):19552-79. [DOI:10.18632/oncotarget.3735] [PMID] [PMCID]
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