Reverse transcriptase-PCR analysis of apoptosis-regulating gene expression in human benign prostatic hyperplasia

Cristiana Angelucci, Fortunata Iacopino, Giovanni Zelano, Gina Lama, Gigliola Sica, Giuseppe Gianesini, Aldo Vittorio Bono

Risultato della ricerca: Contributo in rivistaArticolo in rivistapeer review

11 Citazioni (Scopus)

Abstract

Background: To determine whether an imbalanced interaction between proapototic and antiapoptotic signals may account for the loss of the normal cell growth control in benign prostatic hyperplasia (BPH), the expression of some apoptosisregulating genes (bcl-2, bax, c-myc, fas) was investigated. Patients and Methods: BPH specimens were obtained from 20 patients who underwent trans-urethral resection of the prostate (TURP) or adenomectomy. Gene expression was studied by reverse transcriptase-polymerase chain reaction (RT-PCR) and its correlation with age and serum PSA level was also investigated. Results: Genes were found to be differentially expressed in BPH tissues. In particular, the antiapoptotic gene bcl-2, which was found in 18/20 samples, gave the weakest signal (p<0.05-p<0.001, Wilcoxon’s signed rank test), whereas the cell cycle regulator c-myc was detected in all the specimens and was the most highly expressed (p<0.001). A positive relationship between the expression of bcl-2 and that of the two proapoptotic genes bax and fas was observed (p<0.05, Spearman's rank correlation test), as well as between c-myc and fas levels (p<0.005). Moreover, bax expression positively correlated with age and PSA (p<0.02), which have also been shown to directly correlate (p<0.01). Conclusion: The higher expression of the oncogene c-myc suggests the activation of mitogenic signals within hyperplastic prostate tissue which a relatively high expression of the proapoptotic genes bax and fas fails to counterbalance.
Lingua originaleEnglish
pagine (da-a)3937-3941
Numero di pagine5
RivistaAnticancer Research
Volume25
Stato di pubblicazionePubblicato - 2005

Keywords

  • Benign prostatic hyperplasia, apoptosis, bcl-2, bax, fas, c-myc

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