Circadian biology
CK1ε, PERIOD2, and cancer-selective growth arrest
Open access · cc by · source: Europe PMC
Cancer cells depend more than normal cells on casein kinase 1-epsilon; inhibiting CK1ε causes PERIOD2-dependent growth arrest.
Study at a glance
- Design
- Animal / in-vitro — Kinase shRNA library screen and CK1ε inhibitor assays in isogenic cancer vs normal cells
- N
- Library targets 1,006 genes; cell-line dependency study — no single sample N
- Population
- Isogenic cancer and normal cell models
- Outcome
- Cancer-selective, PERIOD2-dependent growth arrest after CSNK1E/CK1ε inhibition
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
CSNK1E is a cancer-preferential dependency; CK1ε inhibitors phenocopy shRNA, and growth arrest is PERIOD2-dependent.
Methodology
Authors used shRNA and kinase-inhibitor perturbations across isogenic cancer vs normal cell models to find selective dependencies, focusing on CSNK1E/CK1ε and PERIOD2.
Limitations
Not a patient clinical trial of CK1ε drugs; selectivity and potency still need medicinal chemistry.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Multiple empirical papers in this library examine circadian biology with mechanistic biological findings.
Evidence for the claim as stated.
CSNK1E is a cancer-preferential dependency; CK1ε inhibitors phenocopy shRNA, and growth arrest is PERIOD2-dependent.
Evidence for the claim as stated.
Systems and scales differ across circadian biology studies (species, tissues, methods), so mechanisms should not be over-generalised.
Evidence for the claim as stated.
CSNK1E/CK1ε was a cancer-preferential dependency: shRNA and kinase inhibitors phenocopied each other, and growth arrest was PERIOD2-dependent in isogenic cancer versus normal models. That is a selective-dependency result, not a patient trial of CK1ε drugs.
Evidence for the claim as stated.
Loss-of-function tools are not interchangeable. CK1ε used shRNA plus inhibitors in mammalian cancer models; USP8 used Drosophila RNAi; IFN work used receptor knockouts and siRNA in macrophages; PDLP used plant combined KOs. A 'knockdown paper' in flies is not the same genetic lesion as a mouse IFNAR1 knockout or an Arabidopsis double mutant.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Systems and scales differ across circadian biology studies (species, tissues, methods), so mechanisms should not be over-generalised.
- Supports · How does food reset the liver clock?
- Supports · Does light control fungal cellulase genes?
Loss-of-function tools are not interchangeable. CK1ε used shRNA plus inhibitors in mammalian cancer models; USP8 used Drosophila RNAi; IFN work used receptor knockouts and siRNA in macrophages; PDLP used plant combined KOs. A 'knockdown paper' in flies is not the same genetic lesion as a mouse IFNAR1 knockout or an Arabidopsis double mutant.
- Supports · How does USP8 turn on Smoothened?
- Supports · How interferon throttles sterol synthesis in antiviral defense
- Supports · How do proteins find plasmodesmata?
Related papers in this topic
Same topic cluster — not a recommendation engine.