Estrogen activates invasiveness of endometrial cancel cells to the interstitium.
Invasiveness of endometrial cancer cells such as Ishikawa, HEC-1-A and HHUA cells, to the interstitium was significantly enhanced by estradiol, while medroxyprogesterone acetate (MPA) significantly diminished the estradiol-enhanced invasive potential. All of these endometrial cancer cells possess estrogen receptors. It is suggested that invasiveness to the interstitium, and consequently infiltration to the uterine myometrium (which means local advance) are activated by estradiol via a mechanism related to the estrogen receptor, and that MPA as an antiestrogen agent partly inactivates the invasive ability.
Fujimoto
J
J
Department of Obstetrics and Gynecology, Gifu University School of Medicine, Gifu City, Japan.
Hori
M
M
Ichigo
S
S
Morishita
S
S
Tamaya
T
T
D002465:Cell Movement / Q000187:drug effects; D003094:Collagen / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D016889:Endometrial Neoplasms / Q000378:metabolism / Q000473:pathology*; D004958:Estradiol / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D017258:Medroxyprogesterone Acetate / Q000494:pharmacology; D009361:Neoplasm Invasiveness; D011960:Receptors, Estrogen / Q000378:metabolism; D014407:Tumor Cells, Cultured
D004965:Estrogen Antagonists; D011960:Receptors, Estrogen; D004958:Estradiol; D003094:Collagen; D017258:Medroxyprogesterone Acetate