Abstract
Hwang et al. recently showed that VGF substantially contributes to the resistance of human lung cancer cells towards epidermal growth factor receptor kinase inhibitors. This was further linked to enhanced epithelial-mesenchymal transition. Here, we demonstrate that VGF is epigenetically modified in non-small cell lung cancer tissues compared to corresponding tumor-free lung tissues from the same donors by using methylome bead chip analyses. These epigenetic modifications trigger an increased transcription of the VGF gene within the tumors, which then leads to an increased expression of the protein, facilitating epithelial-mesenchymal transition, and the resistance to kinase inhibitors. These results should be taken into account in the design of novel therapeutic and diagnostic approaches.
| Original language | English |
|---|---|
| Article number | 123 |
| Journal | Clinical Epigenetics |
| Volume | 9 |
| Issue number | 1 |
| ISSN | 1868-7075 |
| DOIs | |
| Publication status | Published - 28.11.2017 |
Funding
This work was funded by the German Center for Lung Research (DZL; 82DZL001A5). Human tissues were provided by the BioMaterialBank North, which is funded in part by the Airway Research Center North (ARCN), member of the German Center for Lung Research (DZL), and is member of PopGen 2.0 Network (P2N), which is supported by a grant from the German Ministry for Education and Research (01EY1103).
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
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