MicroRNAs 143 and 145 may be involved in benign prostatic hyperplasia pathogenesis through regulation of target genes and proteins

Carregando...
Imagem de Miniatura
Citações na Scopus
10
Tipo de produção
article
Data de publicação
2014
Título da Revista
ISSN da Revista
Título do Volume
Editora
WICHTIG EDITORE
Citação
INTERNATIONAL JOURNAL OF BIOLOGICAL MARKERS, v.29, n.3, p.E246-E252, 2014
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Objectives: The aim of this study was to analyze the roles of miR-143 and miR-145, as well as the gene and protein expression of their targets (KRAS, ERK5, MAP3K3, and MAP4K4) in the pathogenesis of benign prostatic hyperplasia (BPH). Methods: We analyzed the specimens of 44 patients diagnosed with BPH who underwent surgical treatment. The control group consisted of prostate samples from 2 young patients who were organ donors. miRNAs and their target genes were assessed using real-time polymerase chain reaction (qRT-PCR), and protein levels were assessed by Western blotting. Results: miR-143 and miR-145 were overexpressed in, respectively, 62.5% and 73.8% of the cases. The ERK5 and MAP4K4 genes were underexpressed respectively in 59.4% and 100% of the BPH samples, whereas KRAS and MAP3K3 were overexpressed respectively in 79.4% and 61.5% of the samples. Increased protein expression was found for both KRAS (4,312.2 luminance/area) and MAP3K3 (7,461.7 luminance/area), while the ERK5 protein was more abundant in the samples from patients with prostate larger than 60 grams (p = 0.019). Conclusions: The overexpression of miR-143 and miR-145 in BPH samples suggests an association with the pathogenesis of the disease; additionally, the latter miRNA may act through the inhibition of MAP4K4. KRAS and MAP3K3 overexpression may also be associated with BPH pathogenesis. Further analyses are necessary to confirm these results.
Palavras-chave
Benign prostatic hyperplasia, miRNA, Pathogenesis, Target genes, Target proteins
Referências
  1. Ahmad I, 2013, BRIT J CANCER, V108, P149, DOI 10.1038/bjc.2012.510
  2. Ambros V, 2004, NATURE, V431, P350, DOI 10.1038/nature02871
  3. Bianchi-Frias D, 2010, PLOS ONE, V5, DOI 10.1371/journal.pone.0012501
  4. Boettger T, 2009, J CLIN INVEST, V119, P2634, DOI 10.1172/JCI38864
  5. Chagas MA, 2001, BR J UROL, V27, P26
  6. Chen JF, 2009, J CELL SCI, V122, P13, DOI 10.1242/jcs.041723
  7. Clape C, 2009, PLOS ONE, V4, DOI 10.1371/journal.pone.0007542
  8. Cordes KR, 2009, NATURE, V460, P705, DOI 10.1038/nature08195
  9. Elia L, 2009, Cell Death Differ, V16, P1590, DOI 10.1038/cdd.2009.153
  10. Franco-Salinas G, 2010, CLIN PHARMACOKINET, V49, P177, DOI 10.2165/11317580-000000000-00000
  11. Guntur KVP, 2010, J BIOL CHEM, V285, P6595, DOI 10.1074/jbc.M109.068502
  12. Jin Peng, 2010, Zhonghua Nan Ke Xue, V16, P1068
  13. Kranenburg O, 2005, BBA-REV CANCER, V1756, P81, DOI 10.1016/j.bbcan.2005.1
  14. LEE RC, 1993, CELL, V75, P843, DOI 10.1016/0092-8674(93)90529-Y
  15. Lee SKW, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0021249
  16. Long XC, 2011, J BIOL CHEM, V286, P30119, DOI 10.1074/jbc.M111.258814
  17. Lucia MS, 2008, CURR UROL REP, V99, P272
  18. Mehta PB, 2003, ONCOGENE, V22, P1381, DOI 10.1038/sj.onc.1206154
  19. Nishimoto S, 2006, EMBO REP, V7, P782, DOI 10.1038/sj.embor.7400755
  20. Pagliuca A, 2013, ONCOGENE, V32, P4806, DOI 10.1038/onc.2012.495
  21. Pillai RS, 2005, SCIENCE, V309, P1573, DOI 10.1126/science.1115079
  22. Reinhart BJ, 2000, NATURE, V403, P901, DOI 10.1038/35002607
  23. Schauer IG, 2011, DIFFERENTIATION, V82, P200, DOI 10.1016/j.diff.2011.05.007
  24. Son MY, 2008, REPRODUCTION, V136, P423, DOI 10.1530/REP-08-0080
  25. Tang Jie, 2009, Indian J Urol, V25, P312, DOI 10.4103/0970-1591.56179
  26. THEYER G, 1992, LAB INVEST, V66, P96
  27. Wang XF, 2011, J IMMUNOL, V186, P5791, DOI 10.4049/jimmunol.1002127
  28. Xin M, 2009, GENE DEV, V23, P2166, DOI 10.1101/gad.1842409
  29. Yang JH, 2000, NAT GENET, V24, P309, DOI 10.1038/73550
  30. Zhang ZS, 2008, PROSTATE, V68, P508, DOI 10.1002/pros.20722