AI Article Synopsis
- - The relationship between the nucleus and cell cycle changes during cancer progression causes genomic instability, which tumor cells exploit to avoid cell death and treatment resistance.
- - In epithelial ovarian cancer, the overexpression of claudin-4 is linked to increased therapy resistance and helps stabilize the genome by modifying both the nuclear structure and the cell cycle dynamics.
- - Intervention using a claudin mimic peptide and forskolin shows that disrupting claudin-4 enhances the effectiveness of PARP inhibitors by altering the oxidative stress response and impacting genomic stability.
Article Abstract
High-grade serous ovarian carcinoma is marked by chromosomal instability, which can serve to promote disease progression and allow cancer to evade therapeutic insults. The report highlights the role of claudin-4 in regulating genomic instability and proposes a novel therapeutic approach to exploit claudin-4-mediated regulation.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705808 | PMC |
| http://dx.doi.org/10.1158/2767-9764.CRC-24-0558 | DOI Listing |
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