HIF-1alpha induces MXI1 by alternate promoter usage in human neuroblastoma cells.
(2009) In Experimental Cell Research 315(11). p.1924-1936- Abstract
- Adaptation to low oxygen conditions is essential for maintaining homeostasis and viability in oxygen-consuming multi-cellular tissues, including solid tumors. Central in these processes are the hypoxia-inducible transcription factors, HIF-1 and HIF-2, controlling genes involved in e.g. glucose metabolism and neovascularization. Tumor hypoxia and HIF expression have also been associated with a dedifferentiated phenotype and increased aggressiveness. In this report we show that the MAX interactor-1 (MXI1) gene is directly regulated by HIF proteins in neuroblastoma and breast cancer cells. HIF-binding and transactivation were detected within MXI1 gene regulatory sequences in the vicinity of the MXI1-0 promoter, leading to rapid induction of... (More)
- Adaptation to low oxygen conditions is essential for maintaining homeostasis and viability in oxygen-consuming multi-cellular tissues, including solid tumors. Central in these processes are the hypoxia-inducible transcription factors, HIF-1 and HIF-2, controlling genes involved in e.g. glucose metabolism and neovascularization. Tumor hypoxia and HIF expression have also been associated with a dedifferentiated phenotype and increased aggressiveness. In this report we show that the MAX interactor-1 (MXI1) gene is directly regulated by HIF proteins in neuroblastoma and breast cancer cells. HIF-binding and transactivation were detected within MXI1 gene regulatory sequences in the vicinity of the MXI1-0 promoter, leading to rapid induction of the alternate MXI1-0 isoform followed by a long-term induction of both the MXI1-0 and MXI1 isoforms. Importantly, knock-down of MXI1 had limited effect on MYC/MYCN activity under hypoxia, an observation that might be related to the different functional attributes of the two MXI1 isoforms. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1368096
- author
- Löfstedt, Tobias LU ; Fredlund, Erik LU ; Noguera, Rosa ; Navarro, Samuel ; Holmquist Mengelbier, Linda LU ; Beckman, Siv LU ; Påhlman, Sven LU and Axelson, Håkan LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Experimental Cell Research
- volume
- 315
- issue
- 11
- pages
- 1924 - 1936
- publisher
- Academic Press
- external identifiers
-
- wos:000266656000014
- pmid:19254710
- scopus:67049137354
- ISSN
- 1090-2422
- DOI
- 10.1016/j.yexcr.2009.02.015
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Molecular Tumour Biology (013017540), Molecular Medicine (013031200)
- id
- cb53378f-2281-4104-b20e-30d1477a5aea (old id 1368096)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/19254710?dopt=Abstract
- date added to LUP
- 2016-04-01 12:15:00
- date last changed
- 2022-01-27 01:00:54
@article{cb53378f-2281-4104-b20e-30d1477a5aea, abstract = {{Adaptation to low oxygen conditions is essential for maintaining homeostasis and viability in oxygen-consuming multi-cellular tissues, including solid tumors. Central in these processes are the hypoxia-inducible transcription factors, HIF-1 and HIF-2, controlling genes involved in e.g. glucose metabolism and neovascularization. Tumor hypoxia and HIF expression have also been associated with a dedifferentiated phenotype and increased aggressiveness. In this report we show that the MAX interactor-1 (MXI1) gene is directly regulated by HIF proteins in neuroblastoma and breast cancer cells. HIF-binding and transactivation were detected within MXI1 gene regulatory sequences in the vicinity of the MXI1-0 promoter, leading to rapid induction of the alternate MXI1-0 isoform followed by a long-term induction of both the MXI1-0 and MXI1 isoforms. Importantly, knock-down of MXI1 had limited effect on MYC/MYCN activity under hypoxia, an observation that might be related to the different functional attributes of the two MXI1 isoforms.}}, author = {{Löfstedt, Tobias and Fredlund, Erik and Noguera, Rosa and Navarro, Samuel and Holmquist Mengelbier, Linda and Beckman, Siv and Påhlman, Sven and Axelson, Håkan}}, issn = {{1090-2422}}, language = {{eng}}, number = {{11}}, pages = {{1924--1936}}, publisher = {{Academic Press}}, series = {{Experimental Cell Research}}, title = {{HIF-1alpha induces MXI1 by alternate promoter usage in human neuroblastoma cells.}}, url = {{http://dx.doi.org/10.1016/j.yexcr.2009.02.015}}, doi = {{10.1016/j.yexcr.2009.02.015}}, volume = {{315}}, year = {{2009}}, }