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Title:
n-Butylidenephthalide induced apoptosis in the A549 human lung adenocarcinoma cell line by coupled down-regulation of AP-2α and telomerase activity | Acta Pharmacologica Sinica
Description:
To investigate the role of hTERT gene expression and AP-2α in n-butylidenephthalide (n-BP)-induced apoptosis in A549 lung cancer cells. Viability of A549 cells was measured by MTT assay. Protein expression was determined by Western blot. Telomerase activity was measured using the modified telomere repeat amplification protocol (TRAP) assay. Xenograft mice were used as a model system to study the cytotoxic effect of n-BP in vivo. The morphology of tumor was examined by immunohistochemical staining. The growth of A549 lung cancer cells treated with n-BP was significantly inhibited. Telomerase activity and hTERT mRNA expression were determined by telomeric repeat amplification protocol and reverse transcription-polymerase chain reaction, respectively. n-BP inhibited telomerase activity and hTERT mRNA expression in A549 cells while overexpression of hTERT could abolish BP-induced growth inhibition in the A549 cells. We also showed that hTERT promoter activity in the presence of n-BP was mediated via AP-2α. We saw an inhibition of tumor growth when nude mice carrying A549 subcutaneous xenograft tumors were treated with n-BP. Immunohistochemistry of this tumor tissue also showed a decrease in the expression of hTERT. The antiproliferative effects of n-BP on A549 cells in vitro and in vivo suggest a novel clinical application of this compound in the treatment of lung cancers.
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Keywords {🔍}
cells, htert, expression, telomerase, nbp, activity, cancer, article, cell, apα, google, scholar, cas, inhibition, growth, control, treated, human, protein, tumor, lung, figure, apoptosis, treatment, luciferase, μgml, lin, assay, inhibitor, min, nature, china, chen, promoter, data, mice, taiwan, gene, vehicle, effect, vivo, inhibited, incubated, transfected, site, role, mrna, showed, erk, analysis,
Topics {✒️}
nature portfolio permissions reprints privacy policy biotin-labeled p1-ts primer nature 1989 nature 1991 nature advertising expression index ethanol solutions analytical tools yi-lin sophia chen n-bp-inhibited ap-2α expression anti-caspase-3-rabbit monoclonal antibody ap-2alpha transcription factor n-bp inhibited ap-2α italy horng-jyh harn beta-actin monoclonal antibody n-bp-inhibited htert expression activator protein-2alpha expression full size image n-butylidenephthalide attenuates alzheimer' 1l-6-hydroxymethyl-chiro-inositol 2 2-o-methyl-3-o-octadecylcarbonate phosphatidylinositol 3-kinase/akt/gsk3 serine/threonine kinase akt omniscript reverse transcriptase activating enhancer-binding protein-2 ap-2 family consists c-jun-nh2-kinase pi3k/akt/gsk3β inhibitor ly294002 n-butylidenephthalide induced apoptosis chyou-wei wei pci-neo-hest2-ha8 wen-liang chang contributed human cutaneous melanoma contained ap-2α motif chai-yi lin ap-2α binding sites shinn-zong lin ap-2α sites resulted pgl3-basic luciferase vector bp-induced growth inhibition lung cancer development n-bp-induced apoptosis n-bp induced apoptosis dna-binding protein complexes ap-2α binding site extracellular signal-regulated kinases
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- Is small cell lung cancer the perfect target for anti-telomerase treatment?
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headline:n-Butylidenephthalide induced apoptosis in the A549 human lung adenocarcinoma cell line by coupled down-regulation of AP-2α and telomerase activity
description:To investigate the role of hTERT gene expression and AP-2α in n-butylidenephthalide (n-BP)-induced apoptosis in A549 lung cancer cells. Viability of A549 cells was measured by MTT assay. Protein expression was determined by Western blot. Telomerase activity was measured using the modified telomere repeat amplification protocol (TRAP) assay. Xenograft mice were used as a model system to study the cytotoxic effect of n-BP in vivo. The morphology of tumor was examined by immunohistochemical staining. The growth of A549 lung cancer cells treated with n-BP was significantly inhibited. Telomerase activity and hTERT mRNA expression were determined by telomeric repeat amplification protocol and reverse transcription-polymerase chain reaction, respectively. n-BP inhibited telomerase activity and hTERT mRNA expression in A549 cells while overexpression of hTERT could abolish BP-induced growth inhibition in the A549 cells. We also showed that hTERT promoter activity in the presence of n-BP was mediated via AP-2α. We saw an inhibition of tumor growth when nude mice carrying A549 subcutaneous xenograft tumors were treated with n-BP. Immunohistochemistry of this tumor tissue also showed a decrease in the expression of hTERT. The antiproliferative effects of n-BP on A549 cells in vitro and in vivo suggest a novel clinical application of this compound in the treatment of lung cancers.
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