A5065926182- Epigenetics and DNA Methylation
- 14-3-3 protein interactions
- Ubiquitin and proteasome pathways
- Computational Drug Discovery Methods
- Metabolism, Diabetes, and Cancer
- Genomics, phytochemicals, and oxidative stress
- Cancer, Hypoxia, and Metabolism
- Ferroptosis and cancer prognosis
German Cancer Research Center
2020-2025
Heidelberg University
2020-2025
Abstract Epithelial lineage differentiation is pivotal to mammary gland development and it can pause metastasis of breast cancer (BC) by inducing tumor dormancy. To simulate this, we expressed epithelial genes in mesenchymal BC cells. Inducible expression the OVOL metastatic cells suppressed proliferation migration. We found that C1ORF116 , an OVOL’s target, susceptible genetic epigenetic aberrations BC. It regulated steroids functions as a putative autophagy receptor inhibits antioxidants...
Uncontrolled proliferation and altered metabolic reprogramming are hallmarks of cancer. Active glycolysis glutaminolysis characteristic features these required for tumorigenesis. A fine balance between cancer metabolism autophagy is a prerequisite homeostasis within cells. Here we show that glutamate pyruvate transaminase 2 (GPT2), which serves as pivot glutaminolysis, highly upregulated in aggressive breast cancers, particularly the triple-negative subtype. Abrogation this enzyme results...
Targeted therapies have shown striking success in the treatment of cancer over last years. However, their specific effects on an individual tumor appear to be varying and difficult predict. Using integrative modeling approach that combines mechanistic regression modeling, we gained insights into response mechanisms breast cells due different ligand–drug combinations. The multi-pathway model, capturing ERBB receptor signaling as well downstream MAPK PI3K pathways was calibrated time-resolved...