scholarly journals Hypoxia-inducible factor 1 alpha is required for the tumourigenic and aggressive phenotype associated with Rab25 expression in ovarian cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (16) ◽  
pp. 22650-22664 ◽  
Author(s):  
Natividad Gomez-Roman ◽  
Neha Mohan Sahasrabudhe ◽  
Fiona McGregor ◽  
Anthony J. Chalmers ◽  
Jim Cassidy ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Hypoxia Inducible Factor ◽  
Aggressive Phenotype ◽  
Hypoxia Inducible Factor 1

Serum antibodies recognizing hypoxia-inducible factor 1-alpha and platinum sensitivity in ovarian cancer

2014 ◽  
Vol 133 ◽  
pp. 71-72
Author(s):  
M.D. Dao ◽  
K.J. Agnew ◽  
E.M. Swisher ◽  
B.A. Goff ◽  
M.L. Disis ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Hypoxia Inducible Factor ◽  
Serum Antibodies ◽  
Platinum Sensitivity ◽  
Hypoxia Inducible Factor 1

scholarly journals Ginsenoside 20(S)-Rg3 suppresses ovarian cancer migration via hypoxia-inducible factor 1 alpha and nuclear factor-kappa B signals

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769222 ◽  
Author(s):  
Ting Liu ◽  
Le Zhao ◽  
Huilian Hou ◽  
Lu Ding ◽  
Wei Chen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Hypoxia Inducible Factor ◽  
Nuclear Factor ◽  
Strong Inhibitor ◽  
Α Subunit ◽  
Hypoxia Inducible Factor 1Α ◽  
Oxygen Levels ◽  
Hypoxia Inducible Factor 1 ◽  
Cancer Migration

Hypoxia-inducible factor 1 is believed to play a prominent role in the survival and developing progress of cancers. As a result, inhibiting α subunit of hypoxia-inducible factor 1 represents an attractive strategy against tumor. Although hypoxia-inducible factor 1α is a hypoxia-regulated subunit, increasing evidence indicates that hypoxia-inducible factor 1α could stable expression under normoxic conditions, regulated by non-hypoxia-mediated mechanisms. However, there are few strategies to target hypoxia-inducible factor 1α under normoxic conditions. Here, we report that ginsenoside 20(S)-Rg3, one of the main active ingredients in red ginseng, restrains hypoxia-inducible factor 1α expression under normal oxygen levels in human ovarian cancer cell lines, SKOV3 and 3AO, which leads to potently inhibits migration of ovarian cancer in vitro and in vivo. 20(S)-Rg3 could decrease the expression of hypoxia-inducible factor 1α by upregulation of prolyl hydroxylase domain protein 1 to promoting hypoxia-inducible factor 1α ubiquitin–proteasome degradation under normal oxygen levels. Furthermore, 20(S)-Rg3 could attenuate the expression of nuclear factor-κ B, which may be another possible mechanism for 20(S)-Rg3 to block ovarian cancer migration. Taken together, our study suggests that 20(S)-Rg3 is a strong inhibitor of hypoxia-inducible factor 1α, which may provide a novel agent for future treatments for ovarian cancer.

scholarly journals Hyperglycemia-Associated Dysregulation of O-GlcNAcylation and HIF1A Reduces Anticancer Action of Metformin in Ovarian Cancer Cells (SKOV-3)

2018 ◽  
Vol 19 (9) ◽  
pp. 2750 ◽  
Author(s):  
Aneta Rogalska ◽  
Ewa Forma ◽  
Magdalena Bryś ◽  
Agnieszka Śliwińska ◽  
Agnieszka Marczak
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Energy Demand ◽  
Hypoxia Inducible Factor ◽  
Metabolic Stress ◽  
Ovarian Cancer Cells ◽  
Hypoxia Inducible Factor 1 ◽  
Cancer Cell Death ◽  
Chronic Hyperglycemia

Although cancer cells need more glucose than normal cells to maintain energy demand, chronic hyperglycemia induces metabolic alteration that may dysregulate signaling pathways, including the O-GlcNAcylation and HIF1A (Hypoxia-inducible factor 1-alpha) pathways. Metformin was demonstrated to evoke metabolic stress and induce cancer cell death. The aim of this study was to determine the cytotoxic efficiency of metformin on SKOV-3 cells cultured in hyperglycemia and normoglycemia. To identify the potential mechanism, we assessed the expression of O-linked β-N-acetlyglucosamine transferase (OGT) and glycoside hydrolase O-GlcNAcase (OGA), as well as hypoxia-inducible factor 1-alpha (HIF1A) and glucose transporters (GLUT1, GLUT3). SKOV-3 cells were cultured in normoglycaemia (NG, 5 mM) and hyperglycemia (HG, 25 mM) with and without 10 mM metformin for 24, 48, and 72 h. The proliferation rate, apoptotic and necrotic SKOV-3 cell death were evaluated. Real-Time qPCR was employed to determine mRNA expression of OGT, OGA, GLUT1, GLUT3, and HIF1A. Metformin significantly reduced the proliferation of SKOV-3 cells under normal glucose conditions. Whereas, the efficacy of metformin to induce SKOV-3 cell death was reduced in hyperglycemia. Both hyperglycemia and metformin induced changes in the expression of genes involved in the O-GlcNAcylation status and HIF1A pathway. The obtained results suggest that dysregulation of O-GlcNAcylation, and the related HIF1A pathway, via hyperglycemia, is responsible for the decreased cytotoxic efficiency of metformin in human ovarian cancer cells.

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