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3 edition of Hypoxia-induced upregulation of VEGF mRNA in cervical cancer cell lines found in the catalog.

Hypoxia-induced upregulation of VEGF mRNA in cervical cancer cell lines

James Anthony Chiarotto

Hypoxia-induced upregulation of VEGF mRNA in cervical cancer cell lines

by James Anthony Chiarotto

  • 30 Want to read
  • 17 Currently reading

Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

Thesis (M.Sc.) -- University of Toronto, 1998.

SeriesCanadian theses = -- Thèses canadiennes
The Physical Object
FormatMicroform
Pagination1 microfiche : negative. --
ID Numbers
Open LibraryOL20182893M
ISBN 100612407810

  The induction of vascular endothelial growth factor (VEGF) is an essential feature of tumor angiogenesis, and the hypoxia-inducible factor-1 (HIF-1) transcription factor is known to be a key mediator of this process. In colon cancer, the frequently mutated K- ras oncogene also can regulate VEGF expression, but the role that K- ras may play in hypoxia is unknown. Hypoxia induced VEGF Cited by:   Coexpression of IL-6 and VEGF in human cervical cancer. The close association between IL-6 and VEGF revealed above prompted investigation of the expression of IL-6 and VEGF in cervical cancer by:

  Four different gene sets were generated from the hypoxia induced expression changes; genes upregulated in all 3 cell lines, genes upregulated in one of the cell lines and confirmed as hypoxia regulated by the literature, and correspondingly for the downregulated genes Cited by: Results. The expression level of HIF-1α mRNA, which correlated with its protein level, was significantly higher in tumor tissue than in the corresponding nontumor-bearing lung tissue ( × 10 4 ± × 10 4 versus × 10 4 ± × 10 4; p mRNA showed a significantly positive correlation with the mRNA levels of vascular endothelial growth factor and Cited by:

Hypoxia unleashes the invasive and metastatic potential of tumor cells by largely unknown mechanisms. The Met tyrosine kinase, a high affinity receptor for hepatocyte growth factor (HGF), plays a crucial role in controlling invasive growth and is often overexpressed in cancer. Here we show that: (1) hypoxia activates transcription of the met protooncogene, resulting in higher levels of Met; (2 Cited by: A quantitative analysis of the reduction in oxygen levels required to induce up-regulation of vascular endothelial growth factor (VEGF) mRNA in cervical cancer cell lines. (). Vascular permeability factor (vascular endothelial growth factor) expression and angiogenesis in cervical : T Danielsen and E K Rofstad.


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Hypoxia-induced upregulation of VEGF mRNA in cervical cancer cell lines by James Anthony Chiarotto Download PDF EPUB FB2

Hypoxia-Induced Upregulation of VEGF rnRNA in Cervical Cancer Cell Lines Master of Science, James Anthony Chiarotto Department of Medical Biophysics University of Toronto ABSTRACT Malignant cells produce an angiogenesis factor, vascular endothelial growth factor (VEGF), which is upregulated by hypoxia and may increase metastatic : James Anthony Chiarotto.

In contrast, VEGF secretion did not noticeably increase under hypoxia. Of the 10 cell lines, HSC-2 secreted the highest levels of ANG and VEGF under both normoxic and hypoxic conditions. As HSC-2 was also one of the sensitive cell lines for hypoxia-induced up-regulation of ANG, it was therefore chosen, along with SAS, for subsequent by: In the endothelium, HIF-1α promotes expression of VEGF and its receptor VEGF-R2, thereby regulating an autocrine VEGF signaling loop that is vital to endothelial cell survival, proliferation, migration, and tube formation.

56 Accordingly, EC ablation of HIF-1α inhibits xenograft tumor growth due to reduced tumor by:   A quantitative analysis of the reduction in oxygen levels required to induce up-regulation of vascular endothelial growth factor (VEGF) mRNA in cervical cancer cell lines.

J A Chiarotto 1 &Cited by: Abstract Vascular endothelial growth factor (VEGF) is a potent mitogen specific for endothelial expression is dramatically induced by low oxygen tension in a variety of cell types, and it has been suggested to be a key mediator of hypoxia-induced by:   Fig.

2 Increased expression of VEGF mRNA in mouse brain after hypoxic stimulation. Total RNA was extracted from brains of normal mice and mice exposed to 6–12% oxygen for 24 h.

(Upper panel) Northern blots of total RNA sequentially hybridized with a 32 P‐labelled probe for murine VEGF and the ribosomal protein L(Lower panel) Mean and standard deviation (n = 3) of VEGF mRNA Cited by: Background: Hypoxia-inducible factor 1α (HIF-1α) is a transcription factor that plays an important role in tumor growth by regulating the energy metabolism and angiogenesis.

We herein investigated the mRNA expression level of HIF-1α in non-small cell lung cancer (NSCLC) tissues to clarify the imp. Cells respond to hypoxia by shifting cellular processes from general housekeeping functions to activating specialized hypoxia-response pathways.

Oxygen plays an important role in generating ATP to maintain a productive rate of protein synthesis in normoxia. In hypoxia, the rate of the canonical protein synthesis pathway is significantly slowed and impaired due to limited ATP availability Cited by: 3.

These results demonstrate that hypoxia-induced apelin expression might be regulated by HIF-1α in oral squamous cell cancer. Therefore, apelin may play a critical role in angiogenesis during hypoxic tumor progression in OSCC. However, VEGF signaling appears to play a predominant role in hypoxia-induced tumor by: Cell Culture and Transfection.

Mouse BALB/c3T3 lines were grown in DMEM with % FCS. Cells (2 × 10 6) were transfected with 20 μg of plasmid (linearized with ScaI) by CaPO 4 precipitation, grown for 24–48 h, and selected in μg/ml G After 10–12 d, the resulting colonies (containing at least independent clones) were pooled and maintained in μg/ml G sulfate (Life Cited by: Hypoxia and VEGF mRNA Expression in Human Tumors1 Lisa S.

Ziemery, Cameron J. Koch*, Amit Maity*, Deirdre P. Magarelli*, Anna Marie Horan* and Sydney M. Hypoxia-inducible factor-1α (HIF-1α) is overexpressed in many human tumors and their metastases, and is closely associated with a more aggressive tumor phenotype.

In this study, we investigated the effect of resveratrol, a natural product commonly found in grapes and various other fruits, on hypoxia-induced HIF-1α protein accumulation and vascular endothelial growth factor (VEGF) Cited by: This suggests the possibility that the presence of VEGF mRNA might be used as a marker for relevant levels of hypoxia.

Suspension cultures of three human cervical cancer cell lines, SiHa, ME and HeLa, were used to investigate up-regulation of VEGF mRNA levels following exposure to precisely defined oxygen concentrations for 2 or 4 by:   Hypoxia-induced ZEB1 is positively associated with TAM distribution and cervical cancer progression in clinical specimens.

Hypoxia is a hallmark of solid tumours and leads to Cited by: 1. for the very high levels of constitutively expressed VEGF in many cancer cell lines. 37 mediating hypoxia-induced mRNA stability. Mol Biol Cell ; 9(2) for vascular endothelial. Fig. Hypoxia-induced and HIF-dependent ALKBH5 expression mediates a reduction in total RNA m6A levels.

(A) Nine human breast cancer cell lines were exposed to 20% or 1% O 2 for 24 h, and ALKBH5 mRNA levels were determined by RT-qPCR relative to 18S rRNA and normalized to the mean value for MDA-MB cells (MDA) at 20% OCited by:   Exposing cells to hypoxia (% p0 2) for 24 hours induced a significant up-regulation of CSRP2 in all four cell lines (Fig.

1A). Indeed, CSRP2 protein levels increased by about ten times in Cited by: 8. HIF-1α appears to be involved in regulating survivin expression in multiple tumors and hypoxia-induced cancer cell lines [8, 9].

Our previous study also found that both molecules are involved in. Oxygen (O2) deprivation, or hypoxia, has profound effects on cell metabolism and growth. Cells can adapt to low O2 in part through activation of hypoxia-inducible factor (HIF).

We report here that hypoxia inhibits mRNA translation by suppressing multiple key regulators, including eIF2α, eEF2, and the mammalian target of rapamycin (mTOR) effectors 4EBP1, p70S6K, and rpS6, independent of by: coma cell lines and chondrocytes to hypoxia to test the hypotheses (1) that chondrocytes and chondrosar- coma cells respond to hypoxia with an increase in HIF- la protein and VEGF mRNA expression, and (2) that by knocking down HIF-la gene expression, both HIF-lcl protein levels and VEGF mRNA would by:.

In addition, hypoxia-induced upregulation of TF and procoagulant activity has been reported in a variety of cancer types, including, breast cancer [11], ovarian cancer [12], glioma cancer [Hypoxic cultures of both cell lines secreted in elevated levels the VEGFR-3 ligand VEGF-C but not VEGF-D.

Our findings suggest that under hypoxic conditions an autocrine loop between VEGF-C/VEGFR-3 and HIF-1α is possible in breast carcinoma and lung carcinoma but not in colorectal carcinoma cell by: The constitutive level of vascular endothelial growth factor (VEGF) is more important than hypoxia-induced VEGF up-regulation in the angiogenesis of human melanoma xenografts T Cited by: