TITLE:
Basal Cell Proliferation Induced by Chlormadinone Acetate Suggests Stem Cell Transformation of Prostatic Cells
AUTHORS:
Teiichiro Aoyagi, Issei Takizawa, Isao Kuroda
KEYWORDS:
Stem Cell, Prostate, Hormonal Therapy, Epithelial Mesenchymal Transition
JOURNAL NAME:
Journal of Cancer Therapy,
Vol.9 No.3,
March
19,
2018
ABSTRACT: Introduction
and Objective: Epithelial to Mesenchymal transition (EMT) at the
first hormonal therapy is thought to play an essential role in obtaining
castrate resistance for hormone naive prostate cancer. So we studied EMT of
prostatic cells after exposing various hormonal agents using transurethral resection
(TUR) specimens. Patients and Methods: TUR specimens without hormonal
use (4 cases), specimens after three weeks of chlormadinone acetate (CMA) (9 cases), specimens after
average six months of dutasteride (3 cases), and specimens two weeks after
initial use of degarelix (3 cases) were studied using HE and
immunohistochemical staining with prostate specific antigen (PSA), prostatic
stem cell markers such as CD44, CD117, CD133 and Vimentin. Results: Specimens treated with CMA showed acinar dilatation and atrophy of glandular
cells. Specimens treated with dutasteride showed marked decrease of gland and
specimens treated with degarelix showed decrease of glandular cells. PSA was
stained all of the prostatic glandular cells in all specimens. CD44 was stained
at basal cells in normal prostatic tissue without hormones, however in hormone
treated specimens, basal cells elongate and some glandular cells were also
stained by CD44, especially in CMA treated specimens. Only small numbers of
infiltrating cells in interstitial tissue positively stained with CD 117 and CD
133 in all specimens. Vimentin was stained in all mesenchymal interstitial
cells. Conclusion: Elongation of basal cells and increased sensitivity
to CD44 in glandular cells, especially treated with CMA, were thought to the
result of EMT of prostatic glandular cells.