Sulfonated Styrene-Acrylic Acid Copolymers with pH-Indicator Property

In this study, a polymer pH-indicator was synthesized by sulfonation of poly(styrene-co-acrylic acid) with concentrated sulfuric acid. The synthesized polymer pH-indicator exhibited pH-responsive color changes in aqueous solutions, being purple in alkaline medium (pH 9). The sulfonation process extent and polymer color were affected by time and temperature of the process, as well as acrylic acid (AA) content. The addition of acrylic acid was a crucial point for color change due to the facility of cyclic ketone structure to turn into phenol under acidic condition. Compared with low molecule pH-indicators, the sulfonated copolymer was prepared in form of films being repeatedly used as pH-indicator and easily removed from the acid-base medium.</div

Supplementary Table 1 from Breast Cancer Cell Apoptosis with Phytoestrogens Is Dependent on an Estrogen-Deprived State

PDF file - 65K, The sequence of the primers used in the study.</p

Supplementary Figure 4 from Breast Cancer Cell Apoptosis with Phytoestrogens Is Dependent on an Estrogen-Deprived State

PDF file - 41K, Anti-estrogen, ICI 182 780 blocks phytoestrogen inhibited growth MCF7:5C cells were treated with E2(1nM), equilin (1nM), phytoestrogens (1microM) in presence of various concentrations of ICI 182 780. Total DNA was assessed in each well using a fluorescent DNA quantification kit.</p

Supplementary Figure 3 from Breast Cancer Cell Apoptosis with Phytoestrogens Is Dependent on an Estrogen-Deprived State

PDF file - 136K, Diverse effects of E2, equilin and phytoestrogens on cell cycle progression. Distribution of the cells through the cell-cycle phases was analyzed by flow cytometry in cells treated with E2(1nM), equilin (1nM), genistein (1?M), equol (1?M), coumestrol (1?M) or control for 24 h,48h and 72h. The percentage of the cells in each phase is calculated using the ModFit software. The y axis represents the number of cells and FL2-A represents the intensity of propidium iodide.</p

Supplementary Figure 2 from Breast Cancer Cell Apoptosis with Phytoestrogens Is Dependent on an Estrogen-Deprived State

PDF file - 101K, Differential apoptotic effects of E2 equilin and phytoestrogens MCF7:5C cells were treated with control or E2(1nM), equilin (1nM), phytoestrogens (1microM) for 72h and then stained with YO-PRO-1 and propidium iodide and analysed by flow cytometry.</p

Supplementary Figure 5 from Breast Cancer Cell Apoptosis with Phytoestrogens Is Dependent on an Estrogen-Deprived State

PDF file - 32K, ERalpha and ERbeta mRNA levels in MCF7:5C cells MCF7:5C cells were treated with 0.1% ethanol vehicle (control) and total RNA was isolated after 24h and reverse transcribed and ERalpha and ERbeta mRNA levels was obtained using RT-PCR.</p

Supplementary Figure 1 from Breast Cancer Cell Apoptosis with Phytoestrogens Is Dependent on an Estrogen-Deprived State

PDF file - 135K, Chemical structures of estrogens used in the experiments.(A) Steroidal estrogens (B) phytoestrogens.</p

Figure S2 from Targeting Peroxisome Proliferator-Activated Receptor γ to Increase Estrogen-Induced Apoptosis in Estrogen-Deprived Breast Cancer Cells

E2 suppressed the expression of PPARγ target gene ACOX3 in three breast cancer cell lines. MCF-7 cells were transferred from phenol red containing medium to E2-free medium for 3 days. Next, (A) MCF-7, (B) MCF-7:5C, and (C) MCF-7:2A cells were seeded in six-well plates. After 24 hours, cells were treated with a vehicle control (0.1% EtOH) or E2 (1 nM) for 24, 48, 72 hours. Cells were then harvested in TRIzol reagent. ACOX3 expression levels were quantitated using RT-PCR. *P<0.05 compared with control; **P<0.001 compared with control.</p

Supplementary Table S1 from Targeting Peroxisome Proliferator-Activated Receptor γ to Increase Estrogen-Induced Apoptosis in Estrogen-Deprived Breast Cancer Cells

Validation of cell lines</p

Figure S7 from Targeting Peroxisome Proliferator-Activated Receptor γ to Increase Estrogen-Induced Apoptosis in Estrogen-Deprived Breast Cancer Cells

Effects of GW9662 and T0070907 on two LTED breast cancer cells. A, DNA Growth assay of GW9662 in MCF-7:5C cells. Cells were treated with E2 (1 nM), GW9662 (10, 20 µM), or a combination of them for 7 days. Cells were harvested for DNA proliferation assay. **P<0.001. B, DNA Growth assay of GW9662 in MCF-7:2A cells. Cells were treated with E2 (1 nM), GW9662 (10, 20 µM), or a combination of them for 7 days. Cells were harvested for DNA proliferation assay. *P<0.05, **P<0.001. C, MCF-7:5C cells were treated with E2 (1 nM), T0070907 (5 µM), or a combination of them for 4 days. Cells were then harvested in TRIzol reagent. TNFα expression was quantitated by RT-PCR. **P<0.001. D, T0070907 inhibited phosphorylation of Akt in MCF-7:5C cells. Cells were treated with T0070907 (5 µM) for indicated times. Phosphor-Akt and total Akt were detected using Western blotting. E, MCF-7:5C cells were treated with E2 (1 nM), T0070907 (5 µM), or a combination of them for 72 hours. Cells were then harvested in TRIzol reagent. pS2 expression was quantitated by RT-PCR. **P<0.001. F, MCF-7:2A Cells were treated with E2 (1 nM), T0070907 (2.5 µM), or a combination of them for 72 hours. Cells were then harvested in TRIzol reagent. pS2 expression was quantitated by RT-PCR. *P<0.05, **P<0.001.</p