Your browser doesn't support javascript.
loading
Regulation of the HIF switch in human endothelial and cancer cells.
Slawski, Jakub; Jaskiewicz, Maciej; Barton, Anna; Koziol, Sylwia; Collawn, James F; Bartoszewski, Rafal.
Afiliación
  • Slawski J; Department of Biophysics, Faculty of Biotechnology, University of Wroclaw, Wroclaw, Poland.
  • Jaskiewicz M; International Research Agenda 3P, Medicine Laboratory, Medical University of Gdansk, Gdansk, Poland.
  • Barton A; Department of Biophysics, Faculty of Biotechnology, University of Wroclaw, Wroclaw, Poland.
  • Koziol S; Department of Biophysics, Faculty of Biotechnology, University of Wroclaw, Wroclaw, Poland.
  • Collawn JF; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, USA.
  • Bartoszewski R; Department of Biophysics, Faculty of Biotechnology, University of Wroclaw, Wroclaw, Poland. Electronic address: rafal.bartoszewski@uwr.edu.pl.
Eur J Cell Biol ; 103(2): 151386, 2024 Jun.
Article en En | MEDLINE | ID: mdl-38262137
ABSTRACT
Hypoxia-inducible factors (HIFs) are transcription factors that reprogram the transcriptome for cells to survive hypoxic insults and oxidative stress. They are important during embryonic development and reprogram the cells to utilize glycolysis when the oxygen levels are extremely low. This metabolic change facilitates normal cell survival as well as cancer cell survival. The key feature in survival is the transition between acute hypoxia and chronic hypoxia, and this is regulated by the transition between HIF-1 expression and HIF-2/HIF-3 expression. This transition is observed in many human cancers and endothelial cells and referred to as the HIF Switch. Here we discuss the mechanisms involved in the HIF Switch in human endothelial and cancer cells which include mRNA and protein levels of the alpha chains of the HIFs. A major continuing effort in this field is directed towards determining the differences between normal and tumor cell utilization of this important pathway, and how this could lead to potential therapeutic approaches.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Células Endoteliales / Neoplasias Límite: Humans Idioma: En Revista: Eur J Cell Biol Año: 2024 Tipo del documento: Article País de afiliación: Polonia Pais de publicación: Alemania
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Células Endoteliales / Neoplasias Límite: Humans Idioma: En Revista: Eur J Cell Biol Año: 2024 Tipo del documento: Article País de afiliación: Polonia Pais de publicación: Alemania