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forskolin/rintasyöpä
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 97 tuloksia
Forskolin improves sensitivity to doxorubicin of triple negative breast cancer cells via Protein Kinase A-mediated ERK1/2 inhibition.
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Triple negative breast cancer (TNBC) is an invasive, metastatic, highly aggressive tumor. Cytotoxic chemotherapy represents the current treatment for TNBC. However, relapse and chemo-resistance are very frequent. Therefore, new therapeutic approaches that are able to increase the sensitivity to
1,25-Dihydroxycholecalciferol induces an increase in PGE1- and forskolin-stimulated cyclic-AMP production in T47D human breast cancer cell line.
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The effect of 1,25-dihydroxycholecalciferol [1,25(OH)2D3], the active form of vitamin D3, on cell growth, clonogenicity, and cyclic adenosine monophosphate (cAMP) production was examined in human breast cancer cell line T47D. 1,25(OH)2D3 markedly inhibited proliferation of T47D cells in a time- and
Synthesis of novel forskolin isoxazole derivatives with potent anti-cancer activity against breast cancer cell lines.
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Forskolin C1-isoxazole derivatives (3,5-regioisomers) (11a-e, 14, 15a-h and 15, 16a-g) were synthesized regioselectively by adopting 1,3-dipolar cycloadditions. These derivatives were tested using estrogen receptor positive breast cancer cell lines MCF-7 and BT-474. Majority of the compounds
Forskolin increases the effect of everolimus on aromatase inhibitor-resistant breast cancer cells.
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Aromatase inhibitor (AI) resistance is a major obstacle in the treatment of estrogen receptor-positive breast cancer. Everolimus (EVE) ameliorates AI-resistant breast cancer and is therefore used in cancer treatment. However, some patients show resistance to EVE. Here, we used 30 clones of long-term
Diazepam inhibits forskolin-stimulated adenylyl cyclase activity in human tumour cells.
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Previous studies have shown that the benzodiazepine agonist, diazepam, suppresses adenylyl cyclase activity in rat brain, via a G protein-coupled benzodiazepine receptor. Since diazepam binding sites are also present in diverse non-neuronal tissues including tumour cells, its effects on adenylyl
Stimulation or endothelin-1 secretion by human breast cancer cells through protein kinase A activation: a possible novel paracrine loop involving breast fibroblast-derived prostaglandin E2.
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Breast cancer cells secrete endothelin-1 (ET-1), which may act as a paracrine mitogen in breast tumours. The paracrine factors and signal transduction pathways responsible for regulating ET-1 production in breast cancer are unknown. In this study we have examined the involvement of the protein
Role of prostaglandin E2 receptors in migration of murine and human breast cancer cells.
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Aberrant upregulation of COX-2 enzyme resulting in accumulation of PGE2 in a cancer cell environment is a marker for progression of many cancers, including breast cancer. Four subtypes of cell surface receptors (EP1, EP2, EP3, and EP4), which are coupled with different G-proteins, mediate PGE2
Effects of differentiation-inducing agents on maturation of human MCF-7 breast cancer cells.
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The effects of the differentiation inducing agents (DIAS), sodium butyrate (NaBu), retinoic acid (RA), dimethylformamide (DMF), hexamethylene bisacetamide (HMBA), forskolin, and 12-O-tetradecanoylphorbol-13-acetate (TPA), on the growth, morphology, and estrogen receptor (ER) content and epithelial
Differential regulation of insulin-like growth factor-binding protein-3 protease activity in MCF-7 breast cancer cells by estrogen and transforming growth factor-beta1.
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We have examined the regulation of an insulin-like growth factor-binding protein-3 (IGFBP-3) protease secreted by MCF-7 human breast cancer cells using a ligand-binding assay that relies on the decrease in affinity for des(1-3)IGF-I that occurs when IGFBP-3 becomes proteolyzed. IGFBP-3 protease
Aberrant expression of aromatase in breast cancer tissues.
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The expression of aromatase is tissue-specifically regulated through the alternative use of multiple exons 1 and promoters. We analysed expression levels of aromatase mRNA, preferential utilization of multiple exon 1 of the human aromatase gene, and transcriptional regulation of their multiple
Molecular analysis of aberrant expression of aromatase in breast cancer tissues.
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Aromatase mRNA in non-malignant breast tissues was mainly transcribed form skin fibroblast/fetal liver-specific exon 1 (exon 1b) of the aromatase gene. However, in half the cases of breast cancers, switching of the alternative exons 1 from exon 1b to ovary-specific exon 1 (exon 1c) was observed, and
Regulation of c-fos and c-jun expression by calcitonin in human breast cancer cells.
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Breast cancer cells (BCC) have calcitonin (CT) receptors, yet the action of the hormone on these cells is largely unknown. We found that CT produced a strong and transient time- and dose-dependent increase in c-fos mRNA in BCC lines. This event was prevented by a protein kinase A (PKA) inhibitor,
Hydrocortisone and purinergic signaling stimulate sodium/iodide symporter (NIS)-mediated iodide transport in breast cancer cells.
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The sodium/iodide symporter (NIS) mediates a remarkably effective targeted radioiodide therapy in thyroid cancer; this approach is an emerging candidate for treating other cancers that express NIS, whether endogenously or by exogenous gene transfer. Thus far, the only extrathyroidal malignancy known
Retinoic acids differentially regulate NOR-1 and its closely related orphan nuclear receptor genes in breast cancer cell line MCF-7.
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NOR-1, NGFI-B, and Nurr1 are closely related orphan nuclear receptors implicated in diverse biological processes including cell growth and differentiation. We examined the effect of retinoic acids on the expression of these putative transcription factor genes in the breast cancer cell line MCF-7 by
Membrane estrogen receptor-alpha levels in MCF-7 breast cancer cells predict cAMP and proliferation responses.
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BACKGROUND
17beta-estradiol (E2) can rapidly induce cAMP production, but the conditions under which these cAMP levels are best measured and the signaling pathways responsible for the consequent proliferative effects on breast cancer cells are not fully understood. To help resolve these issues, we
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