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. 2020 Dec 19;162(3):bqaa231. doi: 10.1210/endocr/bqaa231

Figure 3.

Figure 3.

Aromatization of 11-ketotestosterone (11KT) elicits an estrogen response. A, 11KT-mediated estrogen-dependent proliferation (100 nM) as measured by a BrdU proliferation assay is inhibited by 1-µM letrozole or fulvestrant in MCF7arom cells (n = 3). **P less than .005; one-way analysis of variance (ANOVA) and Dunnett’s multiple comparisons test, compared to the control set as 100%. B, 11KT-mediated (100 nM) increase in estrogen-dependent gene expression (cathepsin D [CTSD] and progesterone receptor [PR]) is inhibited by 1-µM letrozole or fulvestrant in MCF7arom cells (n = 3). **P less than .005 and ***P less than .001; one-way ANOVA and Dunnett’s multiple comparisons test, compared to the vehicle control set as 1. C, 11KT, but not 11-hydroxytestosterone (11OHT), induce estrogen-dependent proliferation in MCF7arom as measured by a BrdU proliferation assay. *P less than .05 and **P less than .005; one-way ANOVA and Dunnett’s multiple comparisons test, compared to control set as 100%. D, Schematic illustrating the aromatase and ER-dependent estrogen response elicited by 11KT, but not 11OHT. Experiments A, B, and C are represented as mean ± SEM of A and B, 3, or C, 4 independent experiments, each performed in triplicate.