Activation of STAT3 by hypoxia in in vitro models of cervical cancer and endothelial cells

Ruth Elizabeth Garzon Fernandez, Alejandro Ondo-Méndez, Oscar Javier Ortega Recalde

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Introduction. The tumour microenvironment influences the behaviour of cancer cells. In particular, the stimulation of stressful agents, such as hypoxia, becomes a critical factor in the progression and treatment of cancer. The cellular reaction to various stimuli is manifested in the activation of signalling pathways such as JAK/STAT, one of the most important for its effects on cell differentiation and proliferation.
Objective. To evaluate the status of the JAK/STAT pathway by expression or activation of the STAT3 protein in cervical cancer cells (HeLa) and endothelial cells (EA.hy926) subjected to hypoxia.
Materials and methods. The cell lines were subjected to physical (1% O2) or chemical (100 μM desferrioxamine, DFO) hypoxia for two, six and 24 hours. The change in the expression and activation of STAT3 was determined by Western blot and its subcellular location was determined by indirect immunofluorescence.
Results. Hypoxia was evidenced by activation and translocation to the nucleus of HIF-1. Neither physical hypoxia nor chemistry altered the expression of STAT3, but activation did, as demonstrated by its phosphorylation and translocation to the nucleus in the two models under study.
Conclusions. The importance of hypoxia as a stimulus that modifies the activation of the STAT3 protein in HeLa and EA.hy926 cells was highlighted, making it an important element in the design of therapeutic strategies against cancer.

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Original languageSpanish
Pages (from-to)119-130
Number of pages11
JournalBiomédica : revista del Instituto Nacional de Salud
Volume37
Issue number1
DOIs
StatePublished - 2017

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