Overexpressed progesterone receptor form B inhibit invasive activity suppressing matrix metalloproteinases in endometrial carcinoma cells.
In this study, we focused on the influence of progesterone and its receptor in invasion and MMPs on endometrial carcinoma cells. The growth of Ishikawa cells, to which an progesterone receptor form B (PR-B) expressing vector was transfected, was inhibited by progesterone as was the inhibition of the expression of cyclin D1. By invasion assay, in conditions with progesterone, the invasiveness of Ishikawa cells was inhibited as well as the expression of (metalloproteinase) MMP-1, -2, -7 and -9 and Ets-1 decreased. These results suggest that activation of PR-B by progesterone results in tumor suppression by inhibiting cell growth and invasiveness via suppression of the expression of MMPs.
Saito
Tsuyoshi
T
Department of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, S-1, W-16, Chuo-ku, Sapporo 060-8543, Japan. tsaito@sapmed.ac.jp
Mizumoto
Hisanobu
H
Tanaka
Ryoichi
R
Satohisa
Seiro
S
Adachi
Katsuya
K
Horie
Miyabi
M
Kudo
Ryuichi
R
D015415:Biomarkers; D002455:Cell Division / Q000187:drug effects; D019938:Cyclin D1 / Q000187:drug effects / Q000378:metabolism; D016889:Endometrial Neoplasms / Q000201:enzymology* / Q000473:pathology; D005260:Female; D006801:Humans; D061965:Matrix Metalloproteinase Inhibitors; D009361:Neoplasm Invasiveness / Q000517:prevention & control; D011374:Progesterone / Q000494:pharmacology*; D011980:Receptors, Progesterone / Q000378:metabolism*; D014407:Tumor Cells, Cultured
D015415:Biomarkers; D061965:Matrix Metalloproteinase Inhibitors; D011980:Receptors, Progesterone; C097314:progesterone receptor B; D019938:Cyclin D1; D011374:Progesterone