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[Impact of hypoxia on taxol-induced apoptosis in human ovarian cancer cell line A2780 and its mechanism].
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OBJECTIVE
Hypoxia, a feature and important living microenvironment of solid tumors, might be related to drug-resistance of tumors. This study was to establish a hypoxic model of ovarian cancer cell line A2780, and to investigate impacts of hypoxia and hypoxia inducible factor-1alpha (HIF-1alpha) on
Taxol-induced unfolded protein response activation in breast cancer cells exposed to hypoxia: ATF4 activation regulates autophagy and inhibits apoptosis.
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Understanding the mechanisms responsible for the resistance against chemotherapy-induced cell death is still of great interest since the number of patients with cancer increases and relapse is commonly observed. Indeed, the development of hypoxic regions as well as UPR (unfolded protein response)
Hypoxia counteracts taxol-induced apoptosis in MDA-MB-231 breast cancer cells: role of autophagy and JNK activation.
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Cancer cell resistance against chemotherapy is still a heavy burden to improve anticancer treatments. Autophagy activation and the development of hypoxic regions within the tumors are known to promote cancer cell resistance. Therefore, we sought to evaluate the role of autophagy and hypoxia on the
Combination of Taxol® and dichloroacetate results in synergistically inhibitory effects on Taxol-resistant oral cancer cells under hypoxia.
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Cancer cells preferentially catalyze glucose through the glycolytic pathway in the presence of adequate oxygen. This phenomenon is known as the Warburg effect. As is the case with numerous cancer therapeutic agents, resistance remains a significant problem when using Taxol® to treat malignancies.
Cytoskeleton mediates inhibition of the fast Na+ current in respiratory brainstem neurons during hypoxia.
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Whole-cell Na+ currents (INa) were recorded in inspiratory neurons in a medullary slice preparation from neonatal mouse that contains the functional respiratory network. Hypoxia and metabolic poisoning with KCN rapidly inhibited INa by reducing the number of Na+ channels available for opening during
[The influence of microtubule intervention drugs on the energy metabolism of myocardial cells after hypoxia].
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OBJECTIVE
To investigate the influence of microtubule intervention drugs on the energy metabolism of myocardial cells after hypoxia.
METHODS
The primary passage of cultured myocardial cells from neonatal rats were divided into A (with hypoxia), B (with hypoxia and administration of 10 micromol/ml
[The influence of microtubule intervention drugs on glycolytic key enzymes in myocardial cells after hypoxia].
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OBJECTIVE
To investigate the influence of microtubule intervention drugs on glycolytic key enzymes in myocardial cells after hypoxia.
METHODS
The primary passage of cultured myocardial cells from neonatal rats were divided into A group (with hypoxia), B group (with hypoxia and administration of l0
Investigational new drug-directed, 5-day repeat dose toxicity study of 4-[3-(2-nitro-1-imidazolyl)-propylamino]-7-chloroquinoline hydrochloride (NLCQ-1, NSC 709257) administered with or without Taxol in Sprague-Dawley rats.
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In pre-clinical studies, 4-[3-(2-nitro-1-imidazolyl)-propylamino]-7-chloroquinoline hydrochloride (NLCQ-1, NSC 709257) is a weak DNA-intercalating, hypoxia-selective cytotoxin with a promising profile as an adjuvant to radio/chemotherapy and it is about to enter phase I clinical trials. The present
Taxol alleviates collagen-induced arthritis in mice by inhibiting the formation of microvessels.
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The objective of the present study is to evaluate the inhibitory effects of taxol (PTX) on angiogenesis in a collagen-induced arthritis (CIA) mouse model. Collagen II (C II) and complete Freund's adjuvant (CFA) were used in C57BL/6 (H-2b) mice to generate the CIA model. Random grouping was performed
Polymorphonuclear leukocyte opsonic receptor expression after hypoxia/reoxygenation.
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We investigated the effects of hypoxia/reoxygenation (H/R) and subsequent stimulation of polymorphonuclear leukocytes (PMNs) with either formyl-methionyl-leucyl-phenylalanine (FMLP) or phorbol myristate acetate (PMA) on CD32, CD16, CD35, and CD11b/CD18 expression and on degranulation and superoxide
Taxol prevents myocardial ischemia-reperfusion injury by inducing JNK-mediated HO-1 expression.
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BACKGROUND
Ischemia/hypoxia and reperfusion impair mitochondria and produce a large amount of reactive oxygen species (ROS), which lead to mitochondrial and brain damage. Furthermore, heme oxygenase-1 (HO-1) as a cytoprotective gene protects cells against ROS-induced cell death in
Sensitization of Carboplatinum- and Taxol-Resistant High-Grade Serous Ovarian Cancer Cells Carrying p53, BRCA1/2 Mutations by Emblica officinalis (Amla) via Multiple Targets.
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Background: Ovarian cancer (OC), the most lethal gynecologic malignancy, is highly resistant to current treatment strategies. High-grade serous epithelial ovarian cancer (HGSOC) cells with increased somatic mutations and genomic instability and the resulting heterogeneous mutant phenotypes
[Study on the influence of hypoxia induced microtubule damage on the opening of mitochondrial permeable transition pore of cardiac myocytes in rat].
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OBJECTIVE
To investigate the influence of hypoxia induced microtubule damage on the opening of mitochondrial permeable transition pore (MPTP)of cardiac myocytes and on the decrease of respiratory function in rat.
METHODS
Primary cultured myocardial cells from 30 neonatal rats were randomized as
Hypoxia induces chemoresistance in ovarian cancer cells by activation of signal transducer and activator of transcription 3.
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Signal transducer and activator of transcription 3 (STAT3) is activated in a variety of human cancers, including ovarian cancer. The molecular mechanism by which the STAT3 is activated in cancer cells is poorly understood. We observed that human ovarian xenograft tumors (A2780) in mice were severely
TMEM45A is essential for hypoxia-induced chemoresistance in breast and liver cancer cells.
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BACKGROUND
Hypoxia is a common characteristic of solid tumors associated with reduced response to radio- and chemotherapy, therefore increasing the probability of tumor recurrence. The aim of this study was to identify new mechanisms responsible for hypoxia-induced resistance in breast cancer
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