Combinatory effects of PBDEs and 17β-estradiol on MCF-7 cell proliferation and apoptosis

2011 ◽  
Vol 63 (1) ◽  
pp. 189-194 ◽  
Author(s):  
Kwiecińska Patrycja ◽  
Wróbel Anna ◽  
Ewa Ł. Gregoraszczuk
Keyword(s):  
Cell Proliferation ◽  
Proliferation And Apoptosis ◽  
17Β Estradiol ◽  
Mcf 7

Effects of Simvastatin on Breast Carcinoma Cell Proliferation and Apoptosis via Transforming Growth Factor-β1/Smad3 Pathway

2021 ◽  
Vol 11 (9) ◽  
pp. 1673-1682
Author(s):  
Feng Wang ◽  
Gengbao Qu ◽  
Baokai Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Breast Carcinoma ◽  
Protein Expression ◽  
Breast Cancer Cell ◽  
Cell Apoptosis ◽  
Carcinoma Cell ◽  
Proliferation And Apoptosis ◽  
Smad3 Protein ◽  
Mcf 7

Objective: To investigate the function and causative role of simvastatin (Sim) in breast carcinoma cell apoptosis as well as proliferation. Methods: 20 breast carcinoma patients requiring surgery were treated with Sim (20 days, 30 mg), and samples of pre-treatment (pre) and post-treatment (post) were acquired. We detected tissue cell proliferation and apoptosis changes and used functional experiments to detect cell proliferation and apoptosis changes after treating not only estrogen receptor (ER)-positive (MCF-7) but also ER-negative cells (MDA-MB-231) with Sim or TGF-β1. Detection of p-Smad3 and total Smad3 protein expression changes was conducted, and we finally used in vivo experiments to assess the influence of Sim on breast tumor growth and drug safety. Results: Immunohistochemistry and TUNEL staining results showed that after treatment with Sim, breast carcinoma cell proliferation decreased and apoptosis increased. Functional experiments results showed that Sim notedly promoted the MDA-MB-231 and MCF-7 cell apoptosis, inhibiting migration, proliferation and epithelial mesenchymal transition. Moreover, TGF-β1 protein expression was strikingly lower in Sim group than that in DMSO group. When TGF-β1 and Sim were combined to use, the inhibitory ability of Sim on breast cancer cell proliferation markedly increased and the capability of TGF-β1 protein inducing p-Smad3 protein increased. In addition, after Sim treatment in mice, the tumor volume became smaller, the pathological changes weakened, and there was no significant effect on liver function and kidney function. Conclusion: Sim participates in breast cancer cell apoptosis and proliferation via regulating TGF-β1/Smad3 signal pathway.

scholarly journals MiR199a is implicated in embryo implantation by regulating Grb10 in rat

Reproduction ◽  
2014 ◽  
Vol 147 (1) ◽  
pp. 91-99 ◽  
Author(s):  
Hong-Fei Xia ◽  
Jing-Li Cao ◽  
Xiao-Hua Jin ◽  
Xu Ma
Keyword(s):  
Cell Proliferation ◽  
Embryo Implantation ◽  
Growth Factor Receptor ◽  
Inverse Association ◽  
Loss Of Function ◽  
Endometrial Stromal Cells ◽  
Proliferation And Apoptosis ◽  
17Β Estradiol

MiR199a was found to be differentially expressed in rat uteri between the prereceptive and receptive phase via microRNA (miRNA) microarray analysis in our previous study. However, the role of miR199a in rat embryo implantation remained unknown. In the study, northern blot results showed that the expression levels of miR199a were higher on gestation days 5 and 6 (g.d.5–6) in rat uteri than on g.d.3–4 and g.d.7–8. In situ localization of miR199a in rat uteri showed that miR199a was mainly localized in the stroma or decidua. The expression of miR199a was not significantly different in the uteri of pseudopregnant rats and evidently increased in the uteri of rats subjected to activation of delayed implantation and experimentally induced decidualization. Treatment with 17β-estradiol or both 17β-estradiol and progesterone significantly diminished miR199a levels. Gain of function of miR199a in endometrial stromal cells isolated from rat uteri inhibited cell proliferation and promoted cell apoptosis. Loss of function of miR199a displayed opposite roles on cell proliferation and apoptosis. Further investigation uncovered a significant inverse association between the expression of miR199a and growth factor receptor-bound protein 10 (Grb10), an imprinted gene, and miR199a could bind to the 3′UTR of Grb10 to inhibit Grb10 translation. In addition, in vivo analysis found that the immunostaining of GRB10 was attenuated in the stroma or decidua from g.d.4 to 6, contrary to the enhancement of miR199a. Collectively, upregulation of miR199a in rat uterus during the receptive phase is regulated by blastocyst activation and uterine decidualization. Enforced miR199a expression suppresses cell proliferation partially through targeting Grb10.

scholarly journals In Vitro Effects of HAS-2 Gene Silencing on the Proliferation and Apoptosis of the MCF-7 Human Breast Cancer Cell Line

2016 ◽  
Vol 40 (3-4) ◽  
pp. 807-817 ◽  
Author(s):  
Hong-Yan Zhang ◽  
Feng Liang ◽  
Fei Wang ◽  
Jian-Wei Zhang ◽  
Li Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Human Breast Cancer ◽  
Cancer Cell Line ◽  
Human Breast Cancer Cell ◽  
Human Breast ◽  
Proliferation And Apoptosis ◽  
Sirna Group ◽  
Number Of Cells ◽  
Mcf 7

Background: Breast cancer is characterized by a distinct metastatic pattern involving the regional lymph nodes, bone marrow, lung and liver. This study is aimed to investigate the effects of silencing the HAS-2 gene on the proliferation and apoptosis of human breast cancer cells. Methods: MCF-7 cells were collected and assigned into control, scrambled siRNA and HAS-2- siRNA groups. After transfection, the morphological changes in the MCF-7 cells were observed using phase contrast microscopy. qRT-PCR and Western blot assays were used to detect the mRNA and protein expression of apoptosis-related proteins. CCK-8 and flow cytometry were performed to evaluate cell proliferation, the cell cycle and apoptosis. Results: In the control and the scrambled siRNA groups, cells grew adhered to the wall and mainly showed a spindle shape with a clear nucleolus. Compared with the control and scrambled siRNA groups, increases in the number of cells in early apoptosis and metaphase cells in apoptosis were observed in the HAS-2-siRNA group. The HAS-2-siRNA group showed decreased expression of HAS-2 relative to that in the control and scrambled siRNA groups. No significant differences in cell proliferation, cell cycle distribution or apoptosis were noted between the control and scrambled siRNA groups. In the HAS-2-siRNA group, the cell proliferation ability decreased significantly, but the number of cells in the G0/G1 stage, the number of apoptotic cells and the expression of caspase-3 and caspase-9 increased significantly. Conclusion: Our findings indicate that HAS-2 gene silencing may inhibit proliferation and promote apoptosis in the MCF-7 human breast cancer cell line.

scholarly journals Cyr61, a Member of the CCN Family, Is Required for MCF-7 Cell Proliferation: Regulation by 17β-Estradiol and Overexpression in Human Breast Cancer

Endocrinology ◽  
2001 ◽  
Vol 142 (6) ◽  
pp. 2540-2548 ◽  
Author(s):  
Deepak Sampath ◽  
Richard C. Winneker ◽  
Zhiming Zhang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Hormonal Regulation ◽  
Egf Receptor ◽  
Critical Role ◽  
Immediate Early ◽  
Mammary Adenocarcinoma ◽  
17Β Estradiol ◽  
Mcf 7

Abstract Cyr61, a member of the CCN (CTGF/Cyr61/NOV) family of growth regulators, is a secreted cysteine-rich proangiogenic factor that has been implicated in tumorigenesis. Previous studies have also demonstrated that Cyr61 is regulated by 17β-estradiol (E2) in the uterus. Therefore, we hypothesized that hormonal regulation of Cyr61 may be important in estrogen-dependent pathogenic processes such as breast tumorigenesis. Our study demonstrates that both Cyr61 messenger RNA and protein are induced by E2 in MCF-7 mammary adenocarcinoma cells that primarily overexpress estrogen receptor α (ERα) in a dose-dependent and immediate early fashion. Cyr61 gene induction by E2 is transcriptionally regulated by ERα as the antiestrogen, ICI 182,780, and actinomycin D blocked induction completely. In addition, Cyr61 is up-regulated in MCF-7 cells by epidermal growth factor (EGF) in an immediate early fashion as well. The functional relevance of steroid induction of Cyr61 in breast cancer cell growth is demonstrated by anti-Cyr61 neutralizing antibodies, which diminished E2 and EGF-dependent DNA synthesis and dramatically reduced E2-driven cell proliferation by more than 70%. Most importantly, Cyr61 is overexpressed in 70% (28 of 40) of breast cancer patients with infiltrating ductal carcinoma and is localized exclusively to hyperplastic ductal epithelial cells. Moreover, the levels of Cyr61 protein are higher in breast tumors that are ER+/EGF receptor+ than those that are ER−/EGF receptor+, suggesting that estrogens may mediate Cyr61 expression in vivo. Collectively, our data suggest that Cyr61 may play a critical role in estrogen- as well as growth factor-dependent breast tumor growth.

scholarly journals H19 lncRNA mediates 17β-estradiol-induced cell proliferation in MCF-7 breast cancer cells

2015 ◽  
Vol 33 (6) ◽  
pp. 3045-3052 ◽  
Author(s):  
HONG SUN ◽  
GUO WANG ◽  
YAN PENG ◽  
YING ZENG ◽  
QIONG-NI ZHU ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
17Β Estradiol ◽  
Mcf 7

scholarly journals Dual Effects of N,N-dimethylformamide on Cell Proliferation and Apoptosis in Breast Cancer

Dose-Response ◽  
2017 ◽  
Vol 15 (4) ◽  
pp. 155932581774445 ◽  
Author(s):  
Jihong Zhang ◽  
Daibing Zhou ◽  
Lingyun Zhang ◽  
Qunbo Lin ◽  
Weimin Ren ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Inhibitory Effect ◽  
High Dose ◽  
Dependent Manner ◽  
Cyclin E1 ◽  
Proliferation And Apoptosis ◽  
Dose Dependent ◽  
Mcf 7

N,N-dimethylformamide (DMF) has been widely used as an organic solvent in industries. DMF is a potential medication. However, the antitumorigenic role of DMF in breast cancer remains unclear. Here, we examined dose-dependent effects of DMF on proliferation and apoptosis in breast cancer MCF-7 and nontumorous MCF-12A cells. We found that DMF had a growth inhibitory effect in MCF-12A cells in a dose-dependent manner. By contrast, however, DMF had dual effects on cell proliferation and apoptosis in MCF-7 cells. DMF at a high dose (100 mM) significantly inhibited MCF-7 cell growth while at a low dose (1 mM) significantly stimulated MCF-7 cell growth (both P < .05). The inhibitory effect of DMF on cell proliferation was accompanied by the decrease of cyclin D1 and cyclin E1 protein expression, leading to the cell cycle arrest at the G0/G1 phase. Furthermore, a high-dose DMF significantly increased the number of early apoptotic cells by increasing cleaved caspase-9 and proapoptotic protein Bax expression and decreased the ratio of Bcl-xL/Bax ( P < .01). Thus, our data demonstrated for the first time that DMF has dual effects on breast cancer cell behaviors depending upon its dose. Caution must be warranted in determining its effective dose for targeting breast cancer.

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