Research programme 02
YB-1, mitotic adaptation and chromosomal instability
We study how YB-1 controls cell division and enables TP53-mutant cancers to tolerate abnormal mitosis, genomic instability and treatment stress.
Central question
Which YB-1-dependent mechanisms allow genomically unstable cancer cells to complete—or survive—abnormal cell division?
Y-box binding protein-1 is a multifunctional DNA- and RNA-binding protein linked to proliferation, stress adaptation and therapy resistance. The laboratory has shown that YB-1 is dynamically regulated during G2 and is required for cytokinesis, connecting its localisation and phosphorylation state to faithful cell division.
Current work extends this biology into YB-1-high, TP53-mutant lung cancer. By testing inhibitors of MPS1, PLK1, RSK and Aurora kinase signalling, the programme asks whether cancers that rely on mitotic adaptation can be selectively sensitised to catastrophic division errors. Complementary pan-cancer analyses place YBX1 expression within proliferative, genomically unstable and clinically aggressive tumour states.
Approaches
- Live-cell and confocal microscopy
- Mitotic and cytokinesis phenotyping
- Short-term drug-response assays
- Clonogenic survival assays
- Protein localisation and phosphorylation analysis
- Targeted mitotic-kinase inhibition
Selected work
- YBX1 Expression Marks Proliferative Tumour States with Context-Dependent Genomic Instability: A Pan-Cancer Analysis (2026)
- Critical Role for Cold Shock Protein YB-1 in Cytokinesis (2020)
- Dephosphorylation of YB-1 is Required for Nuclear Localisation During G2 Phase of the Cell Cycle (2020)