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ovarian neoplasms/hypoxia

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Identifying novel hypoxia-associated markers of chemoresistance in ovarian cancer.

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BACKGROUND Ovarian cancer is associated with poor long-term survival due to late diagnosis and development of chemoresistance. Tumour hypoxia is associated with many features of tumour aggressiveness including increased cellular proliferation, inhibition of apoptosis, increased invasion and
Vascular Endothelial Growth Factor (VEGF) and its transcriptional regulator Hypoxia-inducible Factor 1 (HIF-1) play an important role in the process of angiogenesis in many types of cancer, including ovarian cancer. We have examined whether the DNA-damaging drugs cisplatin and doxorubicin and the

The proliferation, apoptosis, invasion of endothelial-like epithelial ovarian cancer cells induced by hypoxia.

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BACKGROUND Epithelial ovarian cancer is one of the most malignant cancers in women because metastasis occurs in the most of patients by the time of diagnosis. Cancer cells have strong capacity to form angiogenesis or vasculogenic mimicry, which plays the major role in its malignant phenotype.
OBJECTIVE Epithelial ovarian cancer (EOC) can be classified into 5 major histological types. Among them, clear cell adenocarcinoma (CCC) has a poor response to chemotherapy and poor prognosis compared with other histological types. Previously, we reported that the hypoxia-inducible protein 2 (HIG2)

Ginsenoside Rb1 inhibits hypoxia-induced epithelial-mesenchymal transition in ovarian cancer cells by regulating microRNA-25.

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Metastasis frequently occurs in advanced ovarian cancer, which not only leads to substantial mortality but also becomes a major challenge to effective treatment. Epithelial-mesenchymal transition (EMT) is a key mechanism facilitating cancer metastasis. Targeting the EMT process with more efficacious

Ginsenoside 20(S)-Rg3 targets HIF-1α to block hypoxia-induced epithelial-mesenchymal transition in ovarian cancer cells.

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The prognosis of patients with ovarian cancer has remained poor mainly because of aggressive cancer progression. Since epithelial-mesenchymal transition (EMT) is an important mechanism mediating invasion and metastasis of cancer cells, targeting the EMT process with more efficacious and less toxic

Cysteine boosters the evolutionary adaptation to CoCl2 mimicked hypoxia conditions, favouring carboplatin resistance in ovarian cancer.

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Ovarian cancer is the second most common gynaecologic malignancy and the most common cause of death from gynaecologic cancer, especially due to diagnosis at an advanced stage, when a cure is rare. As ovarian tumour grows, cancer cells are exposed to regions of hypoxia. Hypoxia is known to be

miR-210, a modulator of hypoxia-induced epithelial-mesenchymal transition in ovarian cancer cell.

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miR-210 has been found consistently induced by hypoxia and implicated in cancer progression. Despite widespread exploration on miR-210 function, little is known about its action on invasion and metastasis of ovarian cancer. In this study, miR-210 was induced by hypoxia in SKOV3 ovarian cancer cells

Natural antisense transcript of hypoxia-inducible factor 1 regulates hypoxic cell apoptosis in epithelial ovarian cancer.

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Hypoxia is a key stress that triggers apoptosis in various tumors, including epithelial ovarian cancer (EOC). Previous researches identified a hypoxia-upregulated lncRNA named "a natural antisense transcript of hypoxia-inducible factor 1 (aHIF)" in some tumors. However, the

Contribution of FPR and TLR9 to hypoxia-induced chemoresistance of ovarian cancer cells.

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The aim of this study was to investigate the role and mechanisms of the formyl peptide receptor (FPR) and the toll-like receptor 9 (TLR9) in hypoxia-induced chemoresistance of human ovarian cancer cells.SKOV3 cells were exposed to hypoxia for 24 hours, the
The camptothecins, which target the intranuclear enzyme topoisomerase I, have advanced to the forefront of several areas of developmental chemotherapy of cancers. In the present study, we investigated the potential anti-human ovarian cancer effects of NSC606985, a novel and rarely studied

Hypoxia-inducible factor 1alpha (HIF-1alpha) correlated with tumor growth and apoptosis in ovarian cancer.

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The aims of this study were to investigate the hypoxia-inducible factor 1alpha (HIF-1alpha) protein inhibition and tumor growth by a molecular target of rapamycin inhibitor, rapamycin, in xenogeneic transplant model of ovarian cancer and to study the correlation of apoptosis with HIF-1alpha and

[Inhibition of hypoxia-inducible factor 1alpha expression and tumor growth in SKOV3 ovarian cancer model by sirolimus].

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OBJECTIVE To investigate the inhibitory effect of the mammalian target of rapamycin (mTOR) inhibitor, sirolimus on expression of hypoxia-inducible factor (HIF)1alpha protein and growth of ovarian carcinoma in an athymic mouse xenogeneic transplant model of ovarian cancer. METHODS Four groups of

Evaluation of a hypoxia regulated gene panel in ovarian cancer.

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A panel of nine hypoxia regulated genes, selected from a previously published fifty gene panel, was investigated for its ability to predict hypoxic ovarian cancer phenotypes. All nine genes including vascular endothelial growth factor A, glucose transporter 1, phosphoglycerate mutase 1, lactate

[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
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