Protection of 5alpha-dihydrotestosterone against TGF-beta-induced apoptosis in FaO cells and induction of mitosis in HepG2 cells.
Administration of TGF-beta1 to both FaO and HepG2 cells significantly induced apoptosis, particularly in FaO cells. Degradation of genomic DNA in FaO cells was rapidly induced by treatment with TGF-beta1 (5 ng/ml) for only 4 hr. 5alpha-dihydrotestosterone (DHT, 25 nM) alone did not affect any significant changes in cell viability and in nuclei of FaO cells; however, pre-treatment with DHT protected genomic DNA degradation induced by TGF-beta1 for 14 hr. Simultaneous treatment with DHT plus TGF-beta1 (D + T) inhibited TGF-beta-induced apoptosis by approximately 50% in FaO cells. On the other hand, D + T treatment increased mitosis in actively growing HepG2 cells. Thus, it is reasonable to conclude that DHT gives growth advantage to hepatocellular-carcinoma cells by inhibiting TGF-beta-induced DNA fragmentation in FaO cells and by inducting mitosis in HepG2 cells.
Lim
I K
IK
Department of Biochemistry, Ajou University School of Medicine, Suwon, Republic of Korea.
Joo
H J
HJ
Choi
K S
KS
Sueoka
E
E
Lee
M S
MS
Ryu
M S
MS
Fujiki
H
H
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D013196:Dihydrotestosterone / Q000494:pharmacology*; D004347:Drug Interactions; D006801:Humans; D008938:Mitosis / Q000187:drug effects*; D051381:Rats; D013045:Species Specificity; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
D016212:Transforming Growth Factor beta; D013196:Dihydrotestosterone