We are analyzing https://link.springer.com/article/10.1186/1476-4598-6-61.

Title:
Differential effects of hypoxia on etoposide-induced apoptosis according to the cancer cell lines | Molecular Cancer
Description:
Background It is more and more recognized that hypoxia plays a role in the resistance of cancer cells to chemotherapy. However, the mechanisms underlying this resistance still need deeper understanding. The aim of this study was to investigate the effect of hypoxia on this process since hypoxia is one of the hallmarks of tumor environment. Results The effect of hypoxia on the apoptosis induced by etoposide, one drug commonly used in chemotherapy, was investigated using three different cancer cell lines. Gene expression changes were also studied in order to delineate the mechanisms responsible for the hypoxia-induced chemoresistance. We observed that hypoxia differentially influenced etoposide-induced cell death according to the cancer cell type. While hypoxia inhibited apoptosis in hepatoma HepG2 cells, it had no influence in lung carcinoma A549 cells and further enhanced it in breast cancer MCF-7 cells. Etoposide increased p53 activity in all cell lines while hypoxia alone decreased it only in HepG2 cells. Hypoxia had no influence on the etoposide-induced p53 activity in A549, increased p53 abundance in MCF-7 cells but markedly decreased p53 activity in HepG2 cells. Using low density DNA arrays to detect the expression of genes involved in the regulation of apoptosis, etoposide and hypoxia were shown to each influence the expression of numerous genes, many of the ones influenced by etoposide being p53 target genes. Again, the influence of hypoxia on the etoposide-induced changes was different according to the cell type. Conclusion These results evidenced that there was a striking parallelism between the effect of hypoxia on the etoposide-induced p53 stabilization as well as p53 target gene expression and its effect on the etoposide-induced apoptosis according to the cell type. They are very interesting not only because they provide one possible mechanism for the induction of chemoresistance under hypoxic conditions in cells like HepG2 but also because they indicate that not all cell types respond the same way. This knowledge is of importance in designing adequate treatment according to the type of tumors.
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Keywords {🔍}

hypoxia, cells, cell, etoposide, expression, apoptosis, activity, hepg, genes, conditions, protein, pubmed, article, dna, etoposideinduced, google, scholar, gene, mcf, cas, effect, level, hypoxic, results, cancer, incubated, influence, lines, bax, antibody, normoxic, incubation, figure, observed, increase, total, induced, hours, data, death, factor, hif, hifα, detected, performed, decreased, specific, presence, damage, caspase,

Topics {✒️}

alexa fluor-568-conjugated anti-mouse fluorogenic substrate ac-devd-afc rabbit anti-phospho-histone h2ax real-time rt-pcr results real time rt-pcr open access article article download pdf reporter plasmid pg13-luc pg13-luc reporter plasmid martine raes & carine michiels transcription-independent pro-apoptotic functions full size image serum-free co2-independent medium 13 μm ac-devd-afc p53-dependent pro-apoptotic genes post-translational modifications required hypoxia-inducible factor 1alpha preventing trail-induced apoptosis hypoxia-inducible factor 1-dependent mouse anti-hif-1α oxygen-dependent prolyl hydroxylase low-density dna microarray specific anti-parp-1 antibody rabbit anti-p21 antibody anti-hif-1α antibody tgf-beta1 signaling pathway oxygen-dependent asparaginyl hydroxylase prevent p53-dependent transcription double-stranded oligonucleotide p53-responsive promoter driving etoposide-induced cell death hif-1α protein level hif-1α phosphorylation status rabbit igg antibody pro-apoptotic gene transcription etoposide-induced dna damage specific anti-p53 antibodies senior research associate etoposide-induced p53 activity etoposide-induced p53 activation privacy choices/manage cookies fluorogenic group afc etoposide-induced p53 stabilization sheep anti-mouse mouse anti-p53 rabbit anti-p53 pro-survival pathways initiated article presents results authors’ original file dna binding activity

Questions {❓}

Fels DR, Koumenis C: HIF-1alpha and p53: the ODD couple?
Harrison L, Blackwell K: Hypoxia and anemia: factors in decreased sensitivity to radiation therapy and chemotherapy?
Piret JP, Mottet D, Raes M, Michiels C: Is HIF-1alpha a pro- or an anti-apoptotic protein?

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         description:It is more and more recognized that hypoxia plays a role in the resistance of cancer cells to chemotherapy. However, the mechanisms underlying this resistance still need deeper understanding. The aim of this study was to investigate the effect of hypoxia on this process since hypoxia is one of the hallmarks of tumor environment. The effect of hypoxia on the apoptosis induced by etoposide, one drug commonly used in chemotherapy, was investigated using three different cancer cell lines. Gene expression changes were also studied in order to delineate the mechanisms responsible for the hypoxia-induced chemoresistance. We observed that hypoxia differentially influenced etoposide-induced cell death according to the cancer cell type. While hypoxia inhibited apoptosis in hepatoma HepG2 cells, it had no influence in lung carcinoma A549 cells and further enhanced it in breast cancer MCF-7 cells. Etoposide increased p53 activity in all cell lines while hypoxia alone decreased it only in HepG2 cells. Hypoxia had no influence on the etoposide-induced p53 activity in A549, increased p53 abundance in MCF-7 cells but markedly decreased p53 activity in HepG2 cells. Using low density DNA arrays to detect the expression of genes involved in the regulation of apoptosis, etoposide and hypoxia were shown to each influence the expression of numerous genes, many of the ones influenced by etoposide being p53 target genes. Again, the influence of hypoxia on the etoposide-induced changes was different according to the cell type. These results evidenced that there was a striking parallelism between the effect of hypoxia on the etoposide-induced p53 stabilization as well as p53 target gene expression and its effect on the etoposide-induced apoptosis according to the cell type. They are very interesting not only because they provide one possible mechanism for the induction of chemoresistance under hypoxic conditions in cells like HepG2 but also because they indicate that not all cell types respond the same way. This knowledge is of importance in designing adequate treatment according to the type of tumors.
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