STAT3 activation by hypoxia in in vitro models of cervix cancer and endothelial cells
INTRODUCTION: The biological behavior of cancer cells is influenced by the tumor microenvironment in which they develop. In this context, stressor stimuli such as hypoxia are considered critical for tumor development and therapeutic management. Cellular response to various stimuli is evidenced in the activation of intracellular signaling pathways such as JAK/STAT, which is one of the most important for its effects in differentiation and cell proliferation.
OBJECTIVE: To evaluate the condition of the JAK/STAT pathway through the expression/activation of the STAT3 protein in cervix cancer cells (HeLa) and endothelial cells (EA.hy926) subjected to hypoxia.
MATERIAL AND METHODS: Cell lines were subjected to physical (1% O2) or chemical (deferoxamine, DFO, 100 μM) hypoxia for 2, 6 and 24 hours. Changes in the expression and activation of STAT3, and its subcellular localization by indirect immunofluorescence, were determined by western blot.
RESULTS: Hypoxia was evidenced by the activation and translocation to the nucleus of HIF-1. Neither physical nor chemical hypoxia altered STAT3 expression, but it did affect its activation, as seen in its phosphorylation and translocation to the nucleus in the two models under study.
CONCLUSIONS: The present study highlights the importance of hypoxia as a stimulus that modifies the activation of the STAT3 protein in HeLa and EA.hy926 cells, which makes it an important factor in the design of therapeutic strategies against cancer.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2017 |
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| Erschienen: |
2017 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:37 |
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| Enthalten in: |
Biomedica : revista del Instituto Nacional de Salud - 37(2017), 1 vom: 24. Jan., Seite 119-130 |
| Sprache: |
Spanisch |
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| Beteiligte Personen: |
Ortega, Óscar [VerfasserIn] |
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| Links: |
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| Themen: |
Cell hypoxia |
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| Anmerkungen: |
Date Completed 09.01.2018 Date Revised 23.10.2018 published: Electronic Citation Status MEDLINE |
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| doi: |
10.7705/biomedica.v37i2.3225 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM272094838 |
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| 500 | |a Date Completed 09.01.2018 | ||
| 500 | |a Date Revised 23.10.2018 | ||
| 500 | |a published: Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a INTRODUCTION: The biological behavior of cancer cells is influenced by the tumor microenvironment in which they develop. In this context, stressor stimuli such as hypoxia are considered critical for tumor development and therapeutic management. Cellular response to various stimuli is evidenced in the activation of intracellular signaling pathways such as JAK/STAT, which is one of the most important for its effects in differentiation and cell proliferation | ||
| 520 | |a OBJECTIVE: To evaluate the condition of the JAK/STAT pathway through the expression/activation of the STAT3 protein in cervix cancer cells (HeLa) and endothelial cells (EA.hy926) subjected to hypoxia | ||
| 520 | |a MATERIAL AND METHODS: Cell lines were subjected to physical (1% O2) or chemical (deferoxamine, DFO, 100 μM) hypoxia for 2, 6 and 24 hours. Changes in the expression and activation of STAT3, and its subcellular localization by indirect immunofluorescence, were determined by western blot | ||
| 520 | |a RESULTS: Hypoxia was evidenced by the activation and translocation to the nucleus of HIF-1. Neither physical nor chemical hypoxia altered STAT3 expression, but it did affect its activation, as seen in its phosphorylation and translocation to the nucleus in the two models under study | ||
| 520 | |a CONCLUSIONS: The present study highlights the importance of hypoxia as a stimulus that modifies the activation of the STAT3 protein in HeLa and EA.hy926 cells, which makes it an important factor in the design of therapeutic strategies against cancer | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a HeLa cells | |
| 650 | 4 | |a STAT transcription factors | |
| 650 | 4 | |a cell hypoxia | |
| 650 | 4 | |a endothelial cells | |
| 650 | 4 | |a stress, physiological | |
| 650 | 4 | |a tumor microenvironment | |
| 650 | 4 | |a uterine neoplasms | |
| 650 | 7 | |a STAT3 Transcription Factor |2 NLM | |
| 700 | 1 | |a Ondo-Méndez, Alejandro |e verfasserin |4 aut | |
| 700 | 1 | |a Garzón, Ruth |e verfasserin |4 aut | |
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