burkitt lymphoma/hypoxie

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Hypoxia-induced secretion of IL-10 from adipose-derived mesenchymal stem cell promotes growth and cancer stem cell properties of Burkitt lymphoma.

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In this study, we explored how the altered paracrine of adipose mesenchymal stem cells (ADSCs) contributed to the growth and cancer stem cell (CSC) properties of the Burkitt lymphoma cells. Condition mediums from normoxia or hypoxia cultured ADSC (CM-ADSC-N or CM-ADSC-H) were collected, and their

Down-regulation of SENP1 expression increases apoptosis of Burkitt lymphoma cells.

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OBJECTIVE To investigate the effect of down-regulation of Sentrin/SUMO-specific protease 1 (SENP1) expression on the apoptosis of human Burkitt lymphoma cells (Daudi cells) and potential mechanisms. METHODS Short hairpin RNA (shRNA) targeting SENP1 was designed and synthesized and then cloned into a

Hypoxia-inducible factor-1α plays roles in Epstein-Barr virus's natural life cycle and tumorigenesis by inducing lytic infection through direct binding to the immediate-early BZLF1 gene promoter.

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When confronted with poor oxygenation, cells adapt by activating survival signaling pathways, including the oxygen-sensitive transcriptional regulators called hypoxia-inducible factor alphas (HIF-αs). We report here that HIF-1α also regulates the life cycle of Epstein-Barr virus (EBV). Incubation of

Different Mechanisms of Regulation of the Warburg Effect in Lymphoblastoid and Burkitt Lymphoma Cells.

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BACKGROUND The Warburg effect is one of the hallmarks of cancer and rapidly proliferating cells. It is known that the hypoxia-inducible factor 1-alpha (HIF1A) and MYC proteins cooperatively regulate expression of the HK2 and PDK1 genes, respectively, in the Burkitt lymphoma (BL) cell line P493-6,

Aberrant DNA methylation associated with silencing BNIP3 gene expression in haematopoietic tumours.

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Hypoxia is a key factor contributing to the progression of human neoplasias and to the development of resistance to chemotherapy. BNIP3 is a proapoptotic member of the Bcl-2 protein family involved in hypoxia-induced cell death. We evaluated the expression and methylation status of BNIP3 gene to

Imbalanced matriptase pericellular proteolysis contributes to the pathogenesis of malignant B-cell lymphomas.

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Membrane-associated serine protease matriptase is widely expressed by epithelial/carcinoma cells in which its proteolytic activity is tightly controlled by the Kunitz-type protease inhibitor, hepatocyte growth factor activator inhibitor (HAI-1). We demonstrate that, although matriptase is not

Comparative study on radiosensitivities of cultured cell lines derived from several human tumors under hypoxic condition.

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Three human cell lines, Burkitt lymphoma cells (P3HR-1), epidermoid carcinoma cells (HeLa S3-1), and melanoma cells (HMV) were irradiated with 200 kV X-rays under three different oxygen conditions. The values of D0 and D10(-2) were estimated for survival curves, and then the dose-modifying factors

Effect of mitochondrially targeted carboxy proxyl nitroxide on Akt-mediated survival in Daudi cells: Significance of a dual mode of action.

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Vicious cycles of mutations and reactive oxygen species (ROS) generation contribute to cancer progression. The use of antioxidants to inhibit ROS generation promotes cytostasis by affecting the mutation cycle and ROS-dependent survival signaling. However, cancer cells select mutations to elevate ROS

Glycolytic enzyme hexokinase II is a putative therapeutic target in B cell malignant lymphoma.

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Hexokinase II (HXKII) is a key regulator of glucose metabolism that converts glucose to glucose-6-phosphate. Furthermore, HXKII blocks mitochondria-dependent apoptosis by inhibiting the release of cytochrome c. HXKII overexpression is frequently found in several types of cancer and confers

Reactivation of Epstein-Barr Virus By HIF-1α Requires p53

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We previously reported that the cellular transcription factor, HIF-1α, binds a hypoxia-response element (HRE) located within the promoter of Epstein-Barr virus's (EBV's) latent-lytic switch BZLF1 gene, Zp, inducing viral reactivation. Here, EBV-infected cell lines derived from gastric cancers

c-Myc transactivation of LDH-A: implications for tumor metabolism and growth.

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Cancer cells are able to overproduce lactic acid aerobically, whereas normal cells undergo anaerobic glycolysis only when deprived of oxygen. Tumor aerobic glycolysis was recognized about seven decades ago; however, its molecular basis has remained elusive. The lactate dehydrogenase-A gene (LDH-A),

Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B cells.

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Because MYC plays a causal role in many human cancers, including those with hypoxic and nutrient-poor tumor microenvironments, we have determined the metabolic responses of a MYC-inducible human Burkitt lymphoma model P493 cell line to aerobic and hypoxic conditions, and to glucose deprivation,

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