Regulation of colon carcinoma cell invasion by hypoxia-inducible factor 1.

By B. Krishnamachary, S. Berg-Dixon, B. Kelly, F. Agani, D. Feldser, Gloria C. Ferreira, N. Iyer, J. Larusch, B. Pak, P. Taghavi and 1 more. Cancer Research, 2003

676 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c18ffd1d9b0aa9c35522e531ffc450c28a8ec06c

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Citations in the corpus

• Direct regulation of TWIST by HIF-1α promotes metastasis (2008, background): “Results Hypoxia or overexpression of HIF-1α induces EMT Previous results showed that HIF-1α overexpression induces tumour invasion and is associated with repression of E-cadheri”
• Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition. (2007, background): “org Volume 117 Number 12 December 2007 3811 in cancer progression and metastasis (23, 24), and HIF-1 has been identified as a regulator of EMT in several cancer cell lines (25, 26).”
• Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer. (2016, background): “Hypoxia and HIFs contribute to EMT by upregulating transcriptional repressors such as SNAIL (Imai et al., 2003), TWIST (Yang et al., 2008), TCF3, ZFHX1A, and ZFHX1B (Krishnamachary et al., 2006), whose gene products in turn repress CDH1.”
• The role of hypoxia-induced factors in tumor progression. (2004, background): “Systemic responses leading to an elevation in the hemoglobin level, and thus improvement in the O 2 transport capacity of the blood, can support the local mechanisms mentioned within tumors (e.g., through activation of the genes for erythropoietin, transferrin, and transferrin receptors) [6, 13 ].”
• Hypoxia-Inducible Factor-1 (HIF-1) (2006, background): “Hypoxia and HIF-1 induce growth factors, such as insulin-like growth factor-2 (IGF2) and transforming growth factor- (TGF- ) (Feldser et al., 1999; Krishnamachary et al., 2003).”
• Regulation of the Chemokine Receptor CXCR4 by Hypoxia (2003, background): “In line with this hypothesis, recent evidence has been provided that invasive cancer phenotype is associated with Hyp and/or HIF-1 overexpression (54).”
• The role of hypoxia in cancer progression, angiogenesis, metastasis, and resistance to therapy (2015, background): “Moreover, HIF-α contributes to cancer metastasis by altering cancer cell adhesion and motility through regulation of epithelial-to-mesenchymal transition (EMT) and E-cad, ZEB1, -2 and TCF3 expression,(58) as well as migration and invasion abilities through CXCR4,(59) CAIX,(60) LOX,(61) MMP-2, and MM”
• Hypoxia: Importance in tumor biology, noninvasive measurement by imaging, and value of its measurement in the management of cancer therapy (2006, background): “Ex vivo assays have shown that exposure to hypoxia for 24 hours stimulates colon cancer cells to invade normal cells, and HIF-1a overexpression increases invasion under normoxic conditions (Krishnamachary et al. 2003).”
• Targeting HIF-1 for cancer therapy (2003, background): “or cells treated with small interfering RNA that targets HIF1α mRN”
• Hypoxia and hypoxia-inducible factors (HIFs): master regulators of metastasis (2010, background): “motility Basement membrane disruption was shown to be promoted by HIF-1a–dependent upregulation of cathepsin D (CTSD), urokinase-type plasminogen-activator receptor (uPAR), and matrix metalloproteinase-2 (MMP2) through a proteolytic cascade (12).”
• Regulation of cell signalling by uPAR (2010, background): “Tumour hypoxia acts through hypoxia-inducible factor 1α ( HIF1A ) to drive uPAR expression through a hypoxia-responsive element (HRE) in the uPAR promote”