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lung neoplasms/hypoxia
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 1252 tuloksia
Hypoxia can impair doxorubicin resistance of non-small cell lung cancer cells by inhibiting MRP1 and P-gp expression and boosting the chemosensitizing effects of MRP1 and P-gp blockers.
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BACKGROUND
Non-small cell lung cancers (NSCLCs) frequently exhibit resistance to therapeutic drugs, which seriously hampers their treatment. Here, we set out to assess the roles of the multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-gp) in the doxorubicin (DOX) resistance of NSCLC cells,
Nobiletin inhibited hypoxia-induced epithelial-mesenchymal transition of lung cancer cells by inactivating of Notch-1 signaling and switching on miR-200b.
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Epithelial-mesenchymal transition (EMT) is an early step in the process of tumor metastasis. It is well known that tumor microenvironment affects malignancy in various carcinomas; in particular, that hypoxia induces EMT. Deregulated notch signaling also contributes a lot to the development of EMT in
The association of 18F-deoxyglucose (FDG) uptake of PET with polymorphisms in the glucose transporter gene (SLC2A1) and hypoxia-related genes (HIF1A, VEGFA, APEX1) in non-small cell lung cancer. SLC2A1 polymorphisms and FDG-PET in NSCLC patients.
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BACKGROUND
Positron emission tomography imaging of lung cancers with 2-[fluorine-18]-fluoro-2-deoxy-D-glucose is a non-invasive diagnostic, and prognostic tool that measures tumor metabolism. We have analyzed the effect of solute carrier family 2 (facilitated glucose transporter), member 1
[Effects of arsenic trioxide on apoptosis and proliferation of human lung cancer cells under hypoxia].
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OBJECTIVE
To observe the effects of different concentrations of arsenic trioxide (As(2)O(3)) on apoptosis and proliferation of human lung cancer cell line A549 in vitro under hypoxia and normoxia.
METHODS
A549 cells were treated with 0, 1, 2, 4 micromol/L As2O3 for 12, 24 and 48 h under hypoxia (5%
Enhancement of antiangiogenic effects of human canstatin with a hypoxia-regulated transgene vector in lung cancer model.
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Canstatin, a newly identified antiangiogenesis protein, has a potent inhibitory effect on the proliferation and growth of endothelial cells. To enhance the expression and antiangiogenic effects of canstatin in solid tumors, we constructed a eukaryotic expression vector that encodes human canstatin
Hypoxia-mediated autophagic flux inhibits silver nanoparticle-triggered apoptosis in human lung cancer cells.
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Solid tumors are frequently associated with resistance to chemotherapy because the fraction of hypoxic tumor cells is substantial. To understand the underlying mechanism of hypoxia on silver nanoparticle (AgNPs)-induced apoptosis, the expression of hypoxia-inducible factor (HIF)-1α, a hallmark of
[Effect of Hypoxia Inducible Factor-1 Alpha on Brain Metastasis from Lung Cancer and Its Mechanism].
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METHODS
The hypoxia model of A549 lung cancer cells was established.Niclosamide enhances the antitumor effects of radiation by inhibiting the hypoxia-inducible factor-1α/vascular endothelial growth factor signaling pathway in human lung cancer cells.
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Lung cancer is one of the leading causes of cancer-associated mortality, worldwide. The overall survival rate remains low, but progress has been made in improving the diagnosis and treatment of lung cancer over the past decades. Niclosamide, a salicylanilide derivative used for the treatment of
Antiangiogenic therapy using endostatin increases the number of ALDH+ lung cancer stem cells by generating intratumor hypoxia.
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Antiangiogenic therapy is becoming a promising option for cancer treatment. However, many investigations have recently indicated that these therapies may have limited efficacy, and the cancers in most patients eventually develop resistance to these therapies. There is considerable recently acquired
Expression of hypoxia-inducible carbonic anhydrase-9 relates to angiogenic pathways and independently to poor outcome in non-small cell lung cancer.
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Carbonic anhydrase-9 (CA9), a transmembrane enzyme with an extracellular active site, is involved in the reversible metabolism of the carbon dioxide to carbonic acid. Up-regulation of CA by hypoxia and the hypoxia-inducible factor (HIF) pathway has been recently postulated (Wykoff et al. Cancer
[Expression of hypoxia inducible factor 1α and its clinical significance in non-small cell lung cancer].
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BACKGROUND
To explore the expression level and its clinical significance of hypoxia inducible factor 1α (HIF-1α) in non-small cell lung cancer.
METHODS
The expression of HIF-1α was detected in 68 human non-small cell lung cancer samples by immunohistochemistry.
RESULTS
Thirty-nine (57.35%) out of 68
Intermittent hypoxia exacerbates tumor progression in a mouse model of lung cancer.
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The purpose of this study was to evaluate whether obstructive sleep apnea (OSA)-related chronic intermittent hypoxia (CIH) influences lung cancer progression and to elucidate the associated mechanisms in a mouse model of lung cancer. C57/BL6 mice in a CIH group were exposed to intermittent hypoxia
Hypoxia Stimulates the Epithelial-to-Mesenchymal Transition in Lung Cancer Cells Through Accumulation of Nuclear β-Catenin.
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OBJECTIVE
Recent studies implied a significant role of hypoxia-inducible factor-1α (HIF1α) in cell transformation. This study aimed to assess the effects of HIF1α on the epithelial-to-mesenchymal transition (EMT) and tumorigenesis of lung adenocarcinoma cells.
METHODS
Invasion, migration and colony
Aberrant expression and association of VEGF and Dll4/Notch pathway molecules under hypoxia in patients with lung cancer.
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Tumor angiogenesis plays important roles in the pathogenesis and prognosis of lung cancer. Both vascular endothelial growth factor (VEGF) and Dll4/Notch pathways are critical for angiogenesis, whereas their relationship under hypoxia in lung cancer remains unknown. Thus, in the present study, we
Effect of hypoxia-inducible factor-1alpha on transcription of survivin in non-small cell lung cancer.
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BACKGROUND
Survivin is a structurally and functionally unique member of the inhibitor of apoptosis protein (IAP) family. It plays an important role, not only in regulating mitosis but also in inhibiting apoptosis. The current literature contains few reports on the transcriptional regulation of
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