Wnt/β-catenin pathway regulates MGMT gene expression in cancer and inhibition of Wnt signalling prevents chemoresistance.
Malin WickströmCecilia DybergJelena MilosevicChrister EinvikRaul CaleroBaldur SveinbjörnssonEmma SandénAnna DarabiPeter SiesjöMarcel KoolPer KognerNinib BaryawnoJohn Inge JohnsenPublished in: Nature communications (2015)
The DNA repair enzyme O6-methylguanine-DNA methyltransferase (MGMT) is commonly overexpressed in cancers and is implicated in the development of chemoresistance. The use of drugs inhibiting MGMT has been hindered by their haematologic toxicity and inefficiency. As a different strategy to inhibit MGMT we investigated cellular regulators of MGMT expression in multiple cancers. Here we show a significant correlation between Wnt signalling and MGMT expression in cancers with different origin and confirm the findings by bioinformatic analysis and immunofluorescence. We demonstrate Wnt-dependent MGMT gene expression and cellular co-localization between active β-catenin and MGMT. Pharmacological or genetic inhibition of Wnt activity downregulates MGMT expression and restores chemosensitivity of DNA-alkylating drugs in mouse models. These findings have potential therapeutic implications for chemoresistant cancers, especially of brain tumours where the use of temozolomide is frequently used in treatment.
Keyphrases
- gene expression
- cell proliferation
- stem cells
- poor prognosis
- dna repair
- dna methylation
- mouse model
- dna damage
- circulating tumor
- squamous cell carcinoma
- long non coding rna
- epithelial mesenchymal transition
- signaling pathway
- genome wide
- single molecule
- mass spectrometry
- multiple sclerosis
- high resolution
- atomic force microscopy
- dna damage response