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Effect of 17 β‐estradiol on the growth of an estrogen receptor‐positive human esophageal carcinoma cell line
Author(s) -
Utsumi Yasuo,
Nakamura Teruhisa,
Nagasue Naofumi,
Kubota Hirofumi,
Harada Takayuki,
Morikawa Shigeru
Publication year - 1991
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19910501)67:9<2284::aid-cncr2820670913>3.0.co;2-2
Subject(s) - estrogen receptor , estrogen , cell growth , endocrinology , receptor , cell culture , medicine , growth inhibition , in vitro , cytosol , arc (geometry) , cancer research , biology , cancer , biochemistry , breast cancer , genetics , enzyme , geometry , mathematics
Receptors for estrogen and for androgen in the nucleus and cytosol (ERn, ERc, ARn, and ARc, respectively) were studied on two newly established human esophageal carcinoma cell lines, ES‐25C and ES‐8C. ES‐25C was ERn+ (the binding content 4.0 fmol/mg protein, Kd 0.09 nM), ERc‐, ARn‐, and ARc‐. No receptors were found in ES‐8C. Various doses of 17β‐estradiol (E 2 ) were added in vitro to investigate its effect on the growth of these cell lines. No effect of E 2 was observed on ER‐ ES‐8C cell line. The growth of ES‐25C cell was significantly inhibited at the doses of 10 −10 and 10 −12 mol/1 E 2 compared with the control. The doubling time of 10 −12 mol/1 E 2 ‐treated cells was 32 hours whereas that of control was 20 hours. This slower growth was reflected in the deduction of cells in S‐phase utilizing 5‐bromo 2′‐deoxyuridine (BrdU) labeling. The current results strongly suggest that the growth inhibition of ER+ esophageal cancer cell by E 2 is mediated by signal transduction induced by the estrogen‐estrogen receptor system.