er antagonism  (Biosynth Carbosynth)

Journal: Cancers

Article Title: New Promising Steroidal Aromatase Inhibitors with Multi-Target Action on Estrogen and Androgen Receptors for Breast Cancer Treatment.

doi: 10.3390/cancers17020165

Figure Lengend Snippet: Figure 6. The impact of ERα on the effects exerted by AIs 6, 10a and 13. (A) MCF-7aro cell viability effects were determined by MTT assay after treatment over 3 days with T (1 nM) plus AIs (1, 5 and 10 µM) in the presence or absence of ICI (100 nM). (B) ER transactivation assays to explore the effects on ER activation, using VM7Luc4E2 cells incubated with AIs (0.1–10 µM), with (ER antagonism) or without (ER agonism) the hormones T or E2. (C) Effects of AIs 6, 10a and 13 (10 µM) on ERα protein expression. β-actin was used as a loading control, being data of densitometry represented as ERα/β-actin ratio. (D) Effects of AIs 6, 10a and 13 (10 µM) on mRNA transcription of ESR1, TFF1, AREG and EGR3 genes in MCF-7aro cells. The mRNA transcript levels of treated cells were quantified using the housekeeping gene ACTB. Cells without treatment were used as control, to which all results in AI-treated cells were normalized. Cells treated with T plus ICI (100 nM) represented positive control. # (p < 0.05), ## (p < 0.01) and ### (p < 0.001) denote differences in MCF-7aro cells treated with AIs in the absence or presence of ICI, while * (p < 0.05), ** (p < 0.01), and *** (p < 0.001) denote differences of AI-treated cells in relation to control cells (T). On the other hand, the differences of AI-treated cells in contrast to control and in relation to ER agonism are indicated by *** (p < 0.001), while in relation to ER antagonism over T are expressed by &&& (p < 0.001).

Article Snippet: For the experiments, VM7Luc4E2 cells were plated at 4 × 105 cells/mL in 96-well white plates and treated with AIs 6, 10a and 13 (0.1–10 μM) over 24 h, with (ER antagonism) or without (ER agonism) 91.8 pM of E2 or 1 nM of T. For agonism assays, we considered as a positive control cells that were treated with T (781.2 pM–25.6 μM) or E2 (180 fM–367 nM), while for ER antagonism, the positive controls were cells that were treated with raloxifene (12.0 pM–24.5 nM; Biosynth Ltd., Berkshire, UK).

Techniques: MTT Assay, Activation Assay, Incubation, Expressing, Control, Positive Control

Journal: Cancers

Article Title: New Promising Steroidal Aromatase Inhibitors with Multi-Target Action on Estrogen and Androgen Receptors for Breast Cancer Treatment.

doi: 10.3390/cancers17020165

Figure Lengend Snippet: Figure 7. The impact of AR on the effects exerted by AIs 6, 10a and 13. (A) MCF-7aro cell viability effects were determined by MTT assay after treatment, over 3 days, with T (1 nM) plus AIs (1, 5 and 10 µM) in the presence or absence of CDX (1 µM). (B) The AR transactivation assay, AR-EcoScreen™, was used to explore the effects of AIs (0.1–10 µM) with (AR antagonism) or without (AR agonism) R1881 (0.1 nM). (C) Effects of AIs (10 µM) on AR protein expression. β-actin was used as a loading control, being data of densitometry represented as AR/β-actin ratio. Cells without AIs treatment were used as control, to which all results in AI-treated cells were normalized. δ (p < 0.05), δδ (p < 0.01) and δδδ (p < 0.001) denote differences of MCF-7aro cells incubated with AIs in the presence or absence of CDX, while ** (p < 0.01) and *** (p < 0.001) denote differences of AI-treated cells in relation to control cells. On the other hand, the differences of AI-treated cells in contrast to control and in relation to AR agonism, are presented by *** (p < 0.001), whereas in relation to AR antagonism are indicated as & (p < 0.05), && (p < 0.001) and &&& (p < 0.001).

Article Snippet: For the experiments, VM7Luc4E2 cells were plated at 4 × 105 cells/mL in 96-well white plates and treated with AIs 6, 10a and 13 (0.1–10 μM) over 24 h, with (ER antagonism) or without (ER agonism) 91.8 pM of E2 or 1 nM of T. For agonism assays, we considered as a positive control cells that were treated with T (781.2 pM–25.6 μM) or E2 (180 fM–367 nM), while for ER antagonism, the positive controls were cells that were treated with raloxifene (12.0 pM–24.5 nM; Biosynth Ltd., Berkshire, UK).

Techniques: MTT Assay, Transactivation Assay, Expressing, Control, Incubation