FGFR2-triggered autophagy and activation of Nrf-2 reduce breast cancer cell response to anti-ER drugs.
Monika Gorska-ArciszMarta PopedaMarcin BraunDominika PiaseckaJoanna I NowakKamila KitowskaGrzegorz StasilojcMarcin OkrojHanna M RomanskaRafał SądejPublished in: Cellular & molecular biology letters (2024)
This study revealed the unknown role of FGFR2 signalling in activation of autophagy and regulation of the p62/Keap1/Nrf-2 interdependence, which has a negative impact on the response of ER+ BCa cells to anti-ER therapies. The data from in silico analyses suggest that expression of Nrf-2 could act as a marker indicating potential benefits of implementation of anti-FGFR therapy in patients with ER+ BCa, in particular, when used in combination with anti-ER drugs.
Keyphrases
- oxidative stress
- endoplasmic reticulum
- estrogen receptor
- breast cancer cells
- induced apoptosis
- cell death
- endoplasmic reticulum stress
- single cell
- signaling pathway
- healthcare
- primary care
- poor prognosis
- stem cells
- small molecule
- cell proliferation
- cell therapy
- young adults
- climate change
- bone marrow
- deep learning
- long non coding rna
- pi k akt