Daidzein Suppresses Tumor Necrosis Factor-α Induced Migration and Invasion by Inhibiting Hedgehog/Gli1 Signaling in Human Breast Cancer Cells

2014 ◽  
Vol 62 (17) ◽  
pp. 3759-3767 ◽  
Author(s):  
Cheng Bao ◽  
Hyeju Namgung ◽  
Jaehoo Lee ◽  
Hyun-Chang Park ◽  
Jiwon Ko ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Migration And Invasion ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Factor Α ◽  
Necrosis Factor

Amentoflavone inhibits tumor necrosis factor-α induced migration and invasion through AKT/mTOR/S6k1/Hedgehog signaling in human breast cancer

2021 ◽  
Author(s):  
Shuai Qiu ◽  
Yimeng Zhou ◽  
Jin Tae Kim ◽  
Cheng Bao ◽  
Hong Jin Lee ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Human Breast Cancer ◽  
Hedgehog Signaling ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Migration And Invasion ◽  
Human Breast ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Α ◽  
Necrosis Factor

Inflammatory cytokine tumor necrosis factor-α (TNFα) has been demonstrated that can accelerate the progression and metastasis in various carcinoma. In this study, we investigated the effect of amentoflavone on inhibiting...

scholarly journals Estradiol Abrogates Apoptosis in Breast Cancer Cells through Inactivation of BAD: Ras-dependent Nongenomic Pathways Requiring Signaling through ERK and Akt

2004 ◽  
Vol 15 (7) ◽  
pp. 3266-3284 ◽  
Author(s):  
Romaine Ingrid Fernando ◽  
Jay Wimalasena
Keyword(s):  
Breast Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Dominant Negative ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

Estrogens such as 17-β estradiol (E2) play a critical role in sporadic breast cancer progression and decrease apoptosis in breast cancer cells. Our studies using estrogen receptor-positive MCF7 cells show that E2 abrogates apoptosis possibly through phosphorylation/inactivation of the proapoptotic protein BAD, which was rapidly phosphorylated at S112 and S136. Inhibition of BAD protein expression with specific antisense oligonucleotides reduced the effectiveness of tumor necrosis factor-α, H2O2, and serum starvation in causing apoptosis. Furthermore, the ability of E2 to prevent tumor necrosis factor-α-induced apoptosis was blocked by overexpression of the BAD S112A/S136A mutant but not the wild-type BAD. BAD S112A/S136A, which lacks phosphorylation sites for p90RSK1 and Akt, was not phosphorylated in response to E2 in vitro. E2 treatment rapidly activated phosphatidylinositol 3-kinase (PI-3K)/Akt and p90RSK1 to an extent similar to insulin-like growth factor-1 treatment. In agreement with p90RSK1 activation, E2 also rapidly activated extracellular signal-regulated kinase, and this activity was down-regulated by chemical and biological inhibition of PI-3K suggestive of cross talk between signaling pathways responding to E2. Dominant negative Ras blocked E2-induced BAD phosphorylation and the Raf-activator RasV12T35S induced BAD phosphorylation as well as enhanced E2-induced phosphorylation at S112. Chemical inhibition of PI-3K and mitogen-activated protein kinase kinase 1 inhibited E2-induced BAD phosphorylation at S112 and S136 and expression of dominant negative Ras-induced apoptosis in proliferating cells. Together, these data demonstrate a new nongenomic mechanism by which E2 prevents apoptosis.

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