TY - JOUR
T1 - In vitro effects of tamoxifen on UM‐SCC head and neck cancer cell lines
T2 - Correlation with the estrogen and progesterone receptor content
AU - Carey, Thomas
AU - Grenman, Reidar
AU - Virolainen, Erkki
AU - Shapira, Amnon
PY - 1987/1/1
Y1 - 1987/1/1
N2 - Eleven squamous‐cell carcinoma (SCC) cell lines derived from patients with head and neck cancer were tested together with the MCF‐7 breast carcinoma cell line for in vitro growth inhibition by tamoxifen. MCF‐7 is known to contain cytosolic receptors for estrogen (ER), progesterone (PgR), androgen (AR) and glucocorticoid. We have previously reported the ER, PgR and AR contents of these 11 head‐and‐neck SCC cancer lines. Starting from day 3 or 4 after passage, cultures were fed daily with medium containing 5% dextran‐charcoal‐treated fetal bovine serum (D5) and 0, 1, 2.5, 5, 7.5 or 10 μm tamoxifen. Eight of the 11 SCC lines and MCF‐7 showed more than 60% growth inhibition when fed with 5 μm tamoxifen. Of these 8 SCC cell lines, 3 contained both ER and PgR, 4 contained only PgR, and one contained neither receptor. The 3 cell lines that were not inhibited by tamoxifen failed to express either ER or PgR. The action of tamoxifen on the cell lines was further investigated by examining the reversibility and the rate of recovery from tamoxifen‐induced growth inhibition in the presence or absence of estrogen. MCF‐7 and two ER‐ and PgR‐positive SCC cell lines, UM‐SCC‐12 and UM‐SCC‐9, recovered more rapidly when the tamoxifen was replaced with medium containing 17‐beta estradiol (E2) than when it was replaced with D5 medium alone. However, of the other tamoxifen‐inhibited cell lines studied, each recovered equally well whether the tamoxifen was replaced with D5 medium or with D5 medium containing E2. Furthermore, some cell lines spontaneously resumed growth within 4 to 5 days in the presence of tamoxifen if no new tamoxifen was added to the culture dish. This ability is specific for some cell lines, and further study is required to determine its significance.
AB - Eleven squamous‐cell carcinoma (SCC) cell lines derived from patients with head and neck cancer were tested together with the MCF‐7 breast carcinoma cell line for in vitro growth inhibition by tamoxifen. MCF‐7 is known to contain cytosolic receptors for estrogen (ER), progesterone (PgR), androgen (AR) and glucocorticoid. We have previously reported the ER, PgR and AR contents of these 11 head‐and‐neck SCC cancer lines. Starting from day 3 or 4 after passage, cultures were fed daily with medium containing 5% dextran‐charcoal‐treated fetal bovine serum (D5) and 0, 1, 2.5, 5, 7.5 or 10 μm tamoxifen. Eight of the 11 SCC lines and MCF‐7 showed more than 60% growth inhibition when fed with 5 μm tamoxifen. Of these 8 SCC cell lines, 3 contained both ER and PgR, 4 contained only PgR, and one contained neither receptor. The 3 cell lines that were not inhibited by tamoxifen failed to express either ER or PgR. The action of tamoxifen on the cell lines was further investigated by examining the reversibility and the rate of recovery from tamoxifen‐induced growth inhibition in the presence or absence of estrogen. MCF‐7 and two ER‐ and PgR‐positive SCC cell lines, UM‐SCC‐12 and UM‐SCC‐9, recovered more rapidly when the tamoxifen was replaced with medium containing 17‐beta estradiol (E2) than when it was replaced with D5 medium alone. However, of the other tamoxifen‐inhibited cell lines studied, each recovered equally well whether the tamoxifen was replaced with D5 medium or with D5 medium containing E2. Furthermore, some cell lines spontaneously resumed growth within 4 to 5 days in the presence of tamoxifen if no new tamoxifen was added to the culture dish. This ability is specific for some cell lines, and further study is required to determine its significance.
UR - http://www.scopus.com/inward/record.url?scp=0023119358&partnerID=8YFLogxK
U2 - 10.1002/ijc.2910390114
DO - 10.1002/ijc.2910390114
M3 - Article
AN - SCOPUS:0023119358
SN - 0020-7136
VL - 39
SP - 77
EP - 81
JO - International Journal of Cancer
JF - International Journal of Cancer
IS - 1
ER -