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Страница 1 от 135 полученные результаты
BNIP3 protects HepG2 cells against etoposide-induced cell death under hypoxia by an autophagy-independent pathway.
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Tumor hypoxia is a common characteristic of most solid tumors and is correlated with poor prognosis for patients partly because hypoxia promotes resistance to cancer therapy. Hypoxia selects cancer cells that are resistant to apoptosis and allows the onset of mechanisms that promote cancer cells
Resistance of SMMC-7721 hepatoma cells to etoposide in hypoxia is reversed by VEGF inhibitor.
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Hypoxia is associated with resistance to chemotherapy in a number of human cancer types; particularly in hepatocellular carcinoma (HCC), which is a highly vascularized tumor. To develop a potential combination therapy strategy that is capable of overcoming the hypoxia‑induced insensitivity to
Effect of hypoxia-inducible factor-1alpha silencing on the sensitivity of human brain glioma cells to doxorubicin and etoposide.
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Multidrug resistance (MDR) is a significant problem underlying the poor prognosis associated with gliomas. Hypoxia-inducible factor-1alpha (HIF-1alpha) is thought to induce the genes expression involved in MDR. To evaluate the effect of silencing HIF-1alpha in human glioma T98G cells, cells were
Hypoxia induces protection against etoposide-induced apoptosis: molecular profiling of changes in gene expression and transcription factor activity.
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BACKGROUND
it is now well established that hypoxia renders tumor cells resistant to radio- but also chemotherapy. However, few elements are currently available as for the mechanisms underlying this protection.
RESULTS
in this study, physiological hypoxia was shown to inhibit apoptosis induced in
Expression of AGPAT2, an enzyme involved in the glycerophospholipid/triacylglycerol biosynthesis pathway, is directly regulated by HIF-1 and promotes survival and etoposide resistance of cancer cells under hypoxia.
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Hypoxia inducible factor-1 (HIF-1) supports survival of normal cells under low oxygen concentration and cancer cells in the hypoxic tumor microenvironment. This involves metabolic reprogramming via upregulation of glycolysis, downregulation of oxidative phosphorylation and, less well documented,
Differential effect of hypoxia on etoposide-induced DNA damage response and p53 regulation in different cell types.
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Among the main causes of cancer cell resistance to chemotherapy are p53 mutation and hypoxic tumor microenvironment. However, the effect of hypoxia can be very different from one cell type to the other. We studied the effect of hypoxia on the etoposide-induced cell death in two cancer cell lines,
Hypoxia promotes etoposide (VP-16) resistance in neuroblastoma CHP126 cells.
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Hypoxia is widespread in solid tumors as a consequence of poorly structured tumor-derived neovasculature, which is recognized to play a role in the resistance of cancer cells to chemotherapy. Etoposide (VP-16), a drug commonly used in chemotherapy, leads to enhanced accumulation of cell populations
Differential protective effects of varying degrees of hypoxia on the cytotoxicities of etoposide and bleomycin.
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Oxygen is thought to be involved both directly and indirectly in the mechanisms of action of several anti-cancer agents. We studied the effects of various oxygen concentrations on the cytotoxicities of the following drugs: bleomycin (BLM), etoposide (VP-16), doxorubicin (DOX), and mitomycin C (MMC).
Differential effects of hypoxia on etoposide-induced apoptosis according to the cancer cell lines.
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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
Hypoxia-induced decrease in p53 protein level and increase in c-jun DNA binding activity results in cancer cell resistance to etoposide.
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Tumor hypoxia is one of the features of tumor microenvironment that contributes to chemoresistance in particular by cellular adaptations that modulate the apoptotic process. However, the mechanisms involved in this resistance still need deeper understanding. In this study, we investigated the
Hypoxia protects HepG2 cells against etoposide-induced apoptosis via a HIF-1-independent pathway.
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Tumor hypoxia has been described to increase the resistance of cancer cells to radiation therapy and chemotherapy. It also supports the invasiveness and metastatic potential of the tumor. However, few data are available on the transduction pathway set up under hypoxia and leading to this resistance
Hypoxia prevents etoposide-induced DNA damage in cancer cells through a mechanism involving hypoxia-inducible factor 1.
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Intratumoral hypoxia is associated with resistance to therapy in many human cancers, and preexposure of tumor cells to hypoxia confers multidrug resistance. Whereas most anticancer drugs kill proliferating tumor cells by causing DNA damage, a role for hypoxia in the prevention and/or repair of
Chronic hypoxia promotes hypoxia-inducible factor-1alpha-dependent resistance to etoposide and vincristine in neuroblastoma cells.
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Hypoxia is widespread in solid tumors as a consequence of poorly structured tumor-derived neovasculature. Direct measurement of low oxygen levels in a range of adult tumor types has correlated tumor hypoxia with advanced stage, poor response to chemotherapy and radiotherapy, and poor prognosis.
Etoposide and hypoxia do not activate apoptosis of multipotent mesenchymal stromal cells in vitro.
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Incubation of multipotent mesenchymal stromal cells from human adipose tissue with etoposide for 24, 48, and 72 h under standard conditions (20% O(2)), at "physiological" oxygen content (5% O(2)), and under hypoxic conditions (1% O(2)) did not induce cell apoptosis and only slightly increased the
[A case of drug induced pneumonitis caused by oral etoposide].
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We report a case of drug induced pneumonitis caused by oral etoposide. A 63-year-old man was admitted to our hospital in August 1991 because of low grade fever and dyspnea. He underwent right upper lobectomy on Nov. 27th, 1990 for lung cancer (squamous cell carcinoma), and courses of adjuvant
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