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retinoblastoma/hypoxia
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Inhibition of hypoxia-induced apoptosis by modulation of retinoblastoma protein-dependent signaling in cardiomyocytes.
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Apoptotic cell death is an important mode of cell loss contributing to heart dysfunction. To analyze the importance of the E2F-dependent regulation of gene transcription in cardiomyocyte apoptosis, the function of cell cycle factors impinging on the retinoblastoma protein (pRb)/E2F pathway was
Retinoblastoma susceptibility gene product pRB activates hypoxia-inducible factor-1 (HIF-1).
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Hypoxia-inducible factor-1 alpha (HIF-1alpha) constitutes a regulatory subunit of HIF-1, a major transcriptional activator of genes that coordinate physiological and pathological responses towards hypoxia. In order to identify novel interaction partners of HIF-1alpha we have applied T7 phage display
Inhibition of hypoxia inducible factor 1α by siRNA-induced apoptosis in human retinoblastoma cells.
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Hypoxia, which activates the hypoxia inducible factor 1α (HIF-1α), is an essential feature of retinoblastoma (RB) and contributes to poor prognosis and resistance to conventional therapy. In this study, the effect of HIF-1α knockdown by small interfering RNA (siRNA) on cell proliferation, apoptosis,
Recruitment of thyroid hormone receptor/retinoblastoma-interacting protein 230 by the aryl hydrocarbon receptor nuclear translocator is required for the transcriptional response to both dioxin and hypoxia.
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The aryl hydrocarbon receptor nuclear translocator/hypoxia-inducible factor (ARNT/HIF-1 beta) mediates an organism's response to various environmental cues, including those to chemical carcinogens, such as 2,3,7,8-tetrachlorodibenzo-rho-dioxin (TCDD or dioxin), via its formation of a functional
The retinoblastoma protein regulates hypoxia-inducible genetic programs, tumor cell invasiveness and neuroendocrine differentiation in prostate cancer cells.
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Loss of tumor suppressor proteins, such as the retinoblastoma protein (Rb), results in tumor progression and metastasis. Metastasis is facilitated by low oxygen availability within the tumor that is detected by hypoxia inducible factors (HIFs). The HIF1 complex, HIF1α and dimerization partner the
Advanced retinoblastoma treatment: targeting hypoxia by inhibition of the mammalian target of rapamycin (mTOR) in LH(BETA)T(AG) retinal tumors.
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OBJECTIVE
The purpose of this study is to analyze the dose response of the mammalian target of rapamycin (mTOR) inhibitor, rapamycin, on tumor burden and hypoxia, and study the treatment effect on vasculature in LH(BETA)T(AG) retinal tumors.
METHODS
This study was approved by the Institutional
Increased hypoxia following vessel targeting in a murine model of retinoblastoma.
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OBJECTIVE
The purpose of this study was to evaluate the effects of vessel targeting and chemotherapy agents on inducing hypoxic regions in LH(BETA)T(AG) murine retinal tumors. METHODS. Twelve- and 16-week-old LH(BETA)T(AG) transgenic retinoblastoma mice were treated with periocular injections to the
Retinoblastoma protein (Rb) links hypoxia to altered mechanical properties in cancer cells as measured by an optical tweezer.
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Hypoxia modulates actin organization via multiple pathways. Analyzing the effect of hypoxia on the biophysical properties of cancer cells is beneficial for studying modulatory signalling pathways by quantifying cytoskeleton rearrangements. We have characterized the biophysical properties of human
Knockdown of hypoxia-inducible factor-1 alpha reduces proliferation, induces apoptosis and attenuates the aggressive phenotype of retinoblastoma WERI-Rb-1 cells under hypoxic conditions.
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BACKGROUND
Hypoxia-inducible factor-1 alpha (HIF-1α) plays a critical role in tumor cell adaption to hypoxia by inducing the transcription of numerous genes. The role of HIF-1α in malignant retinoblastoma remains unclear. We analyzed the role of HIF-1α in WERI-Rb-1 retinoblastoma cells under hypoxic
Hypoxia induces p53 accumulation in the S-phase and accumulation of hypophosphorylated retinoblastoma protein in all cell cycle phases of human melanoma cells.
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Hypoxia has been shown to induce accumulation of p53 and of hypophosphorylated retinoblastoma protein (pRb) in tumour cells. In this study, the cell cycle dependence of p53 accumulation and pRb hypophosphorylation in four human melanoma cell lines that are wild type for p53 was investigated using
Microarray-based analysis: identification of hypoxia-regulated microRNAs in retinoblastoma cells.
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Hypoxia is an essential feature of retinoblastoma and contributes to poor prognosis and resistance to conventional therapy. MicroRNAs (miRNAs) are small non-coding RNAs involved in a wide variety of biological processes, including cell differentiation, proliferation, death and metabolism. However,
A TRIP230-retinoblastoma protein complex regulates hypoxia-inducible factor-1α-mediated transcription and cancer cell invasion.
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Localized hypoxia in solid tumors activates transcriptional programs that promote the metastatic transformation of cells. Like hypoxia-inducible hyper-vascularization, loss of the retinoblastoma protein (Rb) is a trait common to advanced stages of tumor progression in many metastatic cancers.
Hypoxia inhibits growth, proliferation, and increases response to chemotherapy in retinoblastoma cells.
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Retinoblastoma is a malignant tumor of the retina and the most frequent intraocular cancer in children. Low oxygen tension (hypoxia) is a common phenomenon in advanced retinoblastomas, but its biological effect on retinoblastoma growth is not clearly understood. Here we studied how hypoxia altered
Effects of NF-κB and hypoxia on the biological behavior of Y79 retinoblastoma cells.
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We aimed to investigate the influence of nuclear factor-κB (NF-κB) on the biological behavior of Y79 retinoblastoma cells exposed to hypoxia and its possible mechanism. The cells were administrated with hypoxia, and/or 5 μM pyrrolidine dithiocarbamate (PDTC) (a selective NF-κB inhibitor) to inhibit
Targeting hypoxia, a novel treatment for advanced retinoblastoma.
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OBJECTIVE
The purpose of this study was to evaluate the presence and extent of hypoxia in murine retinoblastoma tumors and the feasibility of targeting hypoxic cells as a novel therapeutic strategy.
METHODS
Hypoxic and vascular areas in LH(BETA)T(AG) mouse retinal tumors were measured using
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