Finasteride targets prostate vascularity by inducing apoptosis and inhibiting cell adhesion of benign and malignant prostate cells

Sutton, Manuel; Yingling, Melissa; Vyas, Ash; Atiemo, Humphrey; Borkowski, Andrew; Jacobs, Stephen C.; Kyprianou, Natasha

doi:10.1002/pros.20444

Cited by 28 publications

(18 citation statements)

References 36 publications

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“…Moreover, the content of steroid in the culture medium when carrying out the treatment with finasteride can be decisive in the study of apoptotic effect of this compound. On the other hand, and in agreement with our data, several authors have established that finasteride induces apoptotic cell death in prostate tissues of rat (13,28) and men (29,30).…”

Section: Discussionsupporting

confidence: 93%

Finasteride induces apoptosis via Bcl-2, Bcl-xL, Bax and caspase-3 proteins in LNCaP human prostate cancer cell line

Golbano

Lóppez-Aparicio²,

Recio³

et al. 2008

Int J Oncol

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Abstract.We investigated the effects of finasteride, a 5α-reductase inhibitor, on cell death machinery through the induction of apoptosis in an in vitro model for prostate cancer. Finasteride treatment of the LNCaP hormone-dependent human prostate cancer cell line caused the loss of cell viability and accelerated apoptosis in a concentration-dependent manner. The contents of immunoreactive procaspase-3 were examined by immunoblot analysis and the results suggest that the apoptosis induced by finasteride involves the increase of caspase-3 activity. Early cell changes that occur during apoptosis are associated with mitochondrial changes mediated by members of the Bcl-2 family of proteins. Therefore, Bcl-2, Bcl-x L and Bax were evaluated by the Western blot analysis. The immunoreactivity for pro-apoptotic Bax was markedly increased whereas antiapoptotic Bcl-2 and Bcl-x L expression was significantly reduced after incubation of cells with finasteride. These findings suggest that finasteride induces apoptosis in LNCaP cells via proteins of the Bcl-2 and caspase family.

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Section: Discussionsupporting

confidence: 93%

Finasteride induces apoptosis via Bcl-2, Bcl-xL, Bax and caspase-3 proteins in LNCaP human prostate cancer cell line

Golbano

Lóppez-Aparicio²,

Recio³

et al. 2008

Int J Oncol

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“…3,4 Previous studies have shown that DHT inhibition cannot persistently and extensively induce apoptosis in prostatic epithelial cells. 5 However, the mechanisms are still largely unknown at present.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of androgen induces autophagy in benign prostate epithelial cells

Wang

et al. 2013

Int J of Urology

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Abbreviations & Acronyms 3-MA = 3-methyladenine 5-ARI = 5-α reductase inhibitor AD = androgen deprivation medium BPH = benign prostatic hyperplasia CM = complete medium DAPI = 4, 6-diamidino-2-phenylindole Objective: 5-α Reductase inhibitor can reduce the volume of benign prostatic hyperplasia by lowering benign prostatic hyperplasia level and consequently inducing epithelial cells apoptosis. The present study investigated whether autophagy and apoptosis of benign prostatic hyperplasia epithelial cells are influenced by low benign prostatic hyperplasia levels. Methods: PWR-1E prostate epithelial cells transfected with GFP-LC3 plasmid were subjected to androgen deprivation conditions. Then the autophagic puncta were evaluated by fluorescence microscopy, and the cellular apoptosis rate was detected by 4, 6-diamidino-2-phenylindole staining after blocking of autophagic process by 3-methyladenine. Furthermore, autophagy status was also determined in hyperplasia prostate tissues from 5-α reductase inhibitor-treated patients by immunohistochemistry. Results: In the androgen deprivation medium, autophagic punta increased markedly in PWR-1E cells, and blockage of autophagy by 3-methyladenine significantly promoted PWR-1E cells' apoptosis rate. In vivo, the expression of LC3 protein (an important autophagic marker) in hyperplasia prostate tissue significantly increased after 5-α reductase inhibitor treatment. Meanwhile, the prostate-specific antigen, as an inner control, decreased. Conclusion: 5-α Reductase inhibitor treatment increases autophagy and possibly decreases the apoptosis of prostate epithelial cells.

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“…7 Finasteride, another 5α-reductase inhibitor, is known to induce apoptosis of the glandular epithelium cells and prostate cancer cells. [8][9][10] Therefore, it is possible that normal capsular structures are destroyed as the structure of the prostate changes, causing inflammation and adhesions. Some BPH patients underwent MRI before and after dutasteride treatment, and findings showed that the surgical capsule was clearly visible before the treatment, and became unclear after 18 months of dutasteride therapy.…”

Section: Discussionmentioning

confidence: 99%

Effects of preoperative dutasteride treatment in holmium laser enucleation of the prostate

et al. 2015

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Objectives: To investigate factors influencing the degree of difficulty in finding and maintaining an appropriate plane on the surgical capsule of the prostate during holmium laser enucleation of the prostate. Methods: A total of 116 men undergoing holmium laser enucleation of the prostate for benign prostate hyperplasia between January 2010 and September 2013 at our hospital were included in this analysis. The degree of difficulty in finding and maintaining the plane of the surgical capsule of the prostate was retrospectively evaluated and graded by using video-based analysis according to newly defined criteria (grade I, least difficult; grade IV, most difficult). Factors influencing the degree of difficulty were investigated. Results: Video analysis was possible in 99 of 116 patients. Decapsulation difficulty in decapsulation was deemed as being grade I in 32 patients, grade II in 31 patients, grade III in 20 patients and grade IV in 16 patients. Preoperative dutasteride therapy was the only factor associated with an increasing level of difficulty in decapsulation during holmium laser enucleation of the prostate. Conclusions: Although preoperative dutasteride therapy effectively reduces intraoperative blood loss, surgeons with limited experience should be careful with the use of dutasteride, because its administration might increase surgical difficulty during holmium laser enucleation of the prostate.

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Finasteride targets prostate vascularity by inducing apoptosis and inhibiting cell adhesion of benign and malignant prostate cells

Abstract: Finasteride can induce prostate apoptosis and reduce tissue vascularity by inhibiting epithelial cell adhesion. This evidence supports that finasteride has apoptotic and anti-angiogenic effects against benign and malignant prostate.

Cited by 28 publications

References 36 publications

Finasteride induces apoptosis via Bcl-2, Bcl-xL, Bax and caspase-3 proteins in LNCaP human prostate cancer cell line

Finasteride induces apoptosis via Bcl-2, Bcl-xL, Bax and caspase-3 proteins in LNCaP human prostate cancer cell line

Inhibition of androgen induces autophagy in benign prostate epithelial cells

Effects of preoperative dutasteride treatment in holmium laser enucleation of the prostate

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