Editorial Comment from Dr Chen to Reduction of prostate cancer incidence by naftopidil, an α1‐adrenoceptor antagonist and transforming growth factor‐β signaling inhibitor

Abstract

To date, the following considerations are our concern for the treatment on prostate cancer (PC) cells and tissues with small molecule drugs: (i) α1A-adrenoceptor antagonist activity; (ii) apoptotic activity on PC cells; (iii) inhibition activity on PC cell growth; (iv) chemical structure with piperazine moiety; (v) low incidence of fibrosis; and (vi) low incidence of PC. In the present article,1 we can see that naftopidil fulfils the requirements as mentioned above. Tamsulosin fails to induce apoptosis or inhibits tumor cell growth in PC cell lines, indicating that it is not suitable for the treatment of PC; but it has limited use for the treatment of benign prostatic hypertrophy-induced urinary obstruction. Although adrenoceptor antagonists, doxazosin and terazosin, both with piperazine moiety in chemistry, could not reduce PC incidence, but less potent than naftopidil, which is characterized with naphzoline base. In contrast, tamsulosin, although selectively binding with α1A receptor, but without significant apoptotic activity on cancer cells. In the present study, the follow up of study ended in December 2010 in patients who continued the same α1-adrenoceptor antagonists without diagnosis of PC have arisen some uncertainty problem. I suggest that patients receive monitoring of serum PSA levels during treatment according to a time schedule provided by the hospital. The relative risk between users and “non-users” of α1-adrenoceptor antagonists was not evaluated, perhaps because of a lack of patients in this study who where “non-users”. However, classification of users who used different α1-adrenoceptor antagonists can be used to compare the risk, as described in the present study. None declared.