Restoration of the prolyl-hydroxylase domain protein-3 oxygen-sensing mechanism is responsible for regulation of HIF2α expression and induction of sensitivity of myeloma cells to hypoxia-mediated apoptosis
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Title
Restoration of the prolyl-hydroxylase domain protein-3 oxygen-sensing mechanism is responsible for regulation of HIF2α expression and induction of sensitivity of myeloma cells to hypoxia-mediated apoptosis
Authors
Keywords
Apoptosis, Hypoxia, Small interfering RNAs, Multiple myeloma, DNA methylation, Flow cytometry, Cloning, Immunoblotting
Journal
PLoS One
Volume 12, Issue 12, Pages e0188438
Publisher
Public Library of Science (PLoS)
Online
2017-12-06
DOI
10.1371/journal.pone.0188438
References
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Note: Only part of the references are listed.- Prolyl Hydroxylase 3 Attenuates MCL-1–Mediated ATP Production to Suppress the Metastatic Potential of Colorectal Cancer Cells
- (2016) Praveenkumar Radhakrishnan et al. CANCER RESEARCH
- A DNA-binding Molecule Targeting the Adaptive Hypoxic Response in Multiple Myeloma Has Potent Antitumor Activity
- (2016) V. S. Mysore et al. MOLECULAR CANCER RESEARCH
- Epigenetic re-expression of HIF-2α suppresses soft tissue sarcoma growth
- (2016) Michael S. Nakazawa et al. Nature Communications
- Metabolic Signature Identifies Novel Targets for Drug Resistance in Multiple Myeloma
- (2015) P. Maiso et al. CANCER RESEARCH
- Distinct breast cancer stem/progenitor cell populations require either HIF1α or loss of PHD3 to expand under hypoxic conditions
- (2015) Oihana Iriondo et al. Oncotarget
- Loss of PHD3 allows tumours to overcome hypoxic growth inhibition and sustain proliferation through EGFR
- (2014) Anne-Theres Henze et al. Nature Communications
- Synergistic Induction of Apoptosis in Multiple Myeloma Cells by Bortezomib and Hypoxia-Activated Prodrug TH-302, In Vivo and In Vitro
- (2013) J. Hu et al. MOLECULAR CANCER THERAPEUTICS
- Mammalian Target of Rapamycin Inhibitors Induce Tumor Cell ApoptosisIn VivoPrimarily by Inhibiting VEGF Expression and Angiogenesis
- (2013) Patrick Frost et al. Journal of Oncology
- The updated biology of hypoxia-inducible factor
- (2012) Samantha N Greer et al. EMBO JOURNAL
- Suppression of Glioma Progression by Egln3
- (2012) Vicki A. Sciorra et al. PLoS One
- Oxygen Sensing, Homeostasis, and Disease
- (2011) Gregg L. Semenza NEW ENGLAND JOURNAL OF MEDICINE
- Aberrant Promoter CpG Methylation Is a Mechanism for Impaired PHD3 Expression in a Diverse Set of Malignant Cells
- (2011) Trenton L. Place et al. PLoS One
- PHD3 regulates differentiation, tumour growth and angiogenesis in pancreatic cancer
- (2010) Y Su et al. BRITISH JOURNAL OF CANCER
- The prolyl-hydroxylase EGLN3 and not EGLN1 is inactivated by methylation in plasma cell neoplasia
- (2009) Eleftheria Hatzimichael et al. EUROPEAN JOURNAL OF HAEMATOLOGY
- Prolyl Hydroxylase-3 Is Down-regulated in Colorectal Cancer Cells and Inhibits IKKβ Independent of Hydroxylase Activity
- (2009) Jing Xue et al. GASTROENTEROLOGY
- Regulation of D-cyclin translation inhibition in myeloma cells treated with mammalian target of rapamycin inhibitors: rationale for combined treatment with extracellular signal-regulated kinase inhibitors and rapamycin
- (2009) P. Frost et al. MOLECULAR CANCER THERAPEUTICS
- Inhibition of hypoxia-inducible factor-1 function enhances the sensitivity of multiple myeloma cells to melphalan
- (2009) Y. Hu et al. MOLECULAR CANCER THERAPEUTICS
- The effect of azacitidine on interleukin-6 signaling and nuclear factor- B activation and its in vitro and in vivo activity against multiple myeloma
- (2008) T. Khong et al. HAEMATOLOGICA
- Abnormal Sympathoadrenal Development and Systemic Hypotension in PHD3-/- Mice
- (2008) T. Bishop et al. MOLECULAR AND CELLULAR BIOLOGY
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