BCL2 and CASP8 regulation by NF-kappaB differentially affect mitochondrial function and cell fate in antiestrogen-sensitive and -resistant breast cancer cells. - Test2 - elhamkhani - TriplyDB

BCL2 and CASP8 regulation by NF-kappaB differentially affect mitochondrial function and cell fate in antiestrogen-sensitive and -resistant breast cancer cells.

BCL2 and CASP8 regulation by NF-kappaB differentially affect mitochondrial function and cell fate in antiestrogen-sensitive and -resistant breast cancer cells.

http://www.wikidata.org/entity/Q30432099

about

Application of metabolomics in drug resistant breast cancer research Cannibalism, cell survival, and endocrine resistance in breast cancer 5-Aza-2-deoxycytidine and trichostatin A increase COUP-TFII expression in antiestrogen-resistant breast cancer cell lines.Down-regulation of Forkhead box protein A1 (FOXA1) leads to cancer stem cell-like properties in tamoxifen-resistant breast cancer cells through induction of interleukin-6 ERK/MAPK regulates ERRγ expression, transcriptional activity and receptor-mediated tamoxifen resistance in ER+ breast cancer.The differential disease regulome IFNgamma restores breast cancer sensitivity to fulvestrant by regulating STAT1, IFN regulatory factor 1, NF-kappaB, BCL2 family members, and signaling to caspase-dependent apoptosis.Dynamic modelling of oestrogen signalling and cell fate in breast cancer cells Tamoxifen increases nuclear respiratory factor 1 transcription by activating estrogen receptor beta and AP-1 recruitment to adjacent promoter binding sites NF-κB signaling is required for XBP1 (unspliced and spliced)-mediated effects on antiestrogen responsiveness and cell fate decisions in breast cancer Genomics of the NF-κB signaling pathway: hypothesized role in ovarian cancer.When is a vesicle not just a vesicle: mitochondrial spheroids and mitochondrial autophagosomes The Role of Interferon Regulatory Factor-1 (IRF1) in Overcoming Antiestrogen Resistance in the Treatment of Breast Cancer.Acquisition of estrogen independence induces TOB1-related mechanisms supporting breast cancer cell proliferation.Anti-estrogen resistance in breast cancer is induced by the tumor microenvironment and can be overcome by inhibiting mitochondrial function in epithelial cancer cells.Endoplasmic reticulum stress, the unfolded protein response, autophagy, and the integrated regulation of breast cancer cell fate.Antitumor activity of celastrol nanoparticles in a xenograft retinoblastoma tumor model Endocrine resistance in breast cancer--An overview and update.Protumor activities of the immune response: insights in the mechanisms of immunological shift, oncotraining, and oncopromotion.Inhibition of the proliferation of acquired aromatase inhibitor-resistant breast cancer cells by histone deacetylase inhibitor LBH589 (panobinostat).The interaction between ER and NFκB in resistance to endocrine therapy.The PI3K inhibitor taselisib overcomes letrozole resistance in a breast cancer model expressing aromatase Pseudomonas toxin pyocyanin triggers autophagy: Implications for pathoadaptive mutations Endoplasmic reticulum stress, the unfolded protein response, and gene network modeling in antiestrogen resistant breast cancer COUP-TFII inhibits NFkappaB activation in endocrine-resistant breast cancer cells.Anordrin Eliminates Tamoxifen Side Effects without Changing Its Antitumor Activity An autocrine inflammatory forward-feedback loop after chemotherapy withdrawal facilitates the repopulation of drug-resistant breast cancer cells Growth inhibitive effect of betulinic acid combined with tripterine on MSB-1 cells and its mechanism.In vitro changes in mitochondrial potential, aggresome formation and caspase activity by a novel 17-β-estradiol analogue in breast adenocarcinoma cells.Proteomic identification of E6AP as a molecular target of tamoxifen in MCF7 cells.NFκB signaling is important for growth of antiestrogen resistant breast cancer cells.Evaluation of the ability of adjuvant tamoxifen-benefit gene signatures to predict outcome of hormone-naive estrogen receptor-positive breast cancer patients treated with tamoxifen in the advanced setting.BRCA1-mimetic compound NSC35446.HCl inhibits IKKB expression by reducing estrogen receptor-α occupancy in the IKKB promoter and inhibits NF-κB activity in antiestrogen-resistant human breast cancer cells.C6-ceramide and targeted inhibition of acid ceramidase induce synergistic decreases in breast cancer cell growth.MicroRNA-134-5p promotes high glucose-induced podocyte apoptosis by targeting bcl-2.ERβ alters the chemosensitivity of luminal breast cancer cells by regulating p53 function.Endocrine Resistance in Breast Cancer

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BCL2 and CASP8 regulation by NF-kappaB differentially affect mitochondrial function and cell fate in antiestrogen-sensitive and -resistant breast cancer cells.

http://www.wikidata.org/entity/Q30432099

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2010 nî lūn-bûn

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2010 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2010 թվականի փետրվարին հրատարակված գիտական հոդված

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2010年の論文

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BCL2 and CASP8 regulation by N ...... resistant breast cancer cells.

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BCL2 and CASP8 regulation by N ...... resistant breast cancer cells.

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BCL2 and CASP8 regulation by N ...... -resistant breast cancer cells

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Ayesha N Shajahan

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P2860

Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice

NF- kappa B2/p100 induces Bcl-2 expression

Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors

Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

The nuclear factor kappa B inhibitor parthenolide restores ICI 182,780 (Faslodex; fulvestrant)-induced apoptosis in antiestrogen-resistant breast cancer cells.

Cancer statistics, 2008

Antiestrogens, aromatase inhibitors, and apoptosis in breast cancer

NF kappa B and interferon regulatory factor 1 physically interact and synergistically induce major histocompatibility class I gene expression

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