RIP140 inhibits glycolysis-dependent proliferation of breast cancer cells by regulating GLUT3 expression through transcriptional crosstalk between hypoxia induced factor and p53.
Breast cancer
Cancer cell metabolism
GLUT3
Glycolysis
HIF
RIP140
Transcription factors
p53
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
03 May 2022
03 May 2022
Historique:
received:
03
01
2022
accepted:
28
03
2022
revised:
18
03
2022
entrez:
2
5
2022
pubmed:
3
5
2022
medline:
6
5
2022
Statut:
epublish
Résumé
Glycolysis is essential to support cancer cell proliferation, even in the presence of oxygen. The transcriptional co-regulator RIP140 represses the activity of transcription factors that drive cell proliferation and metabolism and plays a role in mammary tumorigenesis. Here we use cell proliferation and metabolic assays to demonstrate that RIP140-deficiency causes a glycolysis-dependent increase in breast tumor growth. We further demonstrate that RIP140 reduces the transcription of the glucose transporter GLUT3 gene, by inhibiting the transcriptional activity of hypoxia inducible factor HIF-2α in cooperation with p53. Interestingly, RIP140 expression was significantly associated with good prognosis only for breast cancer patients with tumors expressing low GLUT3, low HIF-2α and high p53, thus confirming the mechanism of RIP140 anti-tumor activity provided by our experimental data. Overall, our work establishes RIP140 as a critical modulator of the p53/HIF cross-talk to inhibit breast cancer cell glycolysis and proliferation.
Identifiants
pubmed: 35501580
doi: 10.1007/s00018-022-04277-3
pii: 10.1007/s00018-022-04277-3
pmc: PMC9061696
doi:
Substances chimiques
Basic Helix-Loop-Helix Transcription Factors
0
Glucose Transporter Type 3
0
NRIP1 protein, human
0
Nuclear Receptor Interacting Protein 1
0
SLC2A3 protein, human
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
270Informations de copyright
© 2022. The Author(s).
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