ArticleOncogene2025
Cyclin E1 overexpression sensitizes ovarian cancer cells to WEE1 and PLK1 inhibition.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Whole-Exome Sequencing Identifies Candidate Genomic Features Associated with Response to Platinum-Based Chemotherapy and Ixabepilone-Based Treatment in Ovarian Cancer.International journal of molecular sciences · 2026Article
- DNA methylation profiling enables subclassification of mucinous ovarian carcinoma and distinguishes it from extraovarian mucinous metastases.Cell reports. Medicine · 2026Article
- Cyclin E1 overexpression identifies a therapeutically relevant poor prognostic patient subgroup in high-grade serous ovarian cancer.NPJ precision oncology · 2026Article
- Impact of Chromosomal Instability and Aneuploidy in Cancer Development.Annual review of cancer biology · 2026Article
- Precision targeting ofTranslational cancer research · 2026Article
- Biomarker-Driven Treatments for Ovarian Cancer: Moving Beyond HRD?International journal of women's health · 2026Review
- PLK1 or WEE1 inhibition targets homologous recombination repair proficiency in BRCA1/2 wild-type high-grade serous ovarian cancer.Cell death & disease · 2025Article
- Clinical relevance of PLK1 in epithelial ovarian cancer.Frontiers in pharmacology · 2025Review
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Authors and funding
18 authors.
Funding
Abstract
Cyclin E1 (CCNE1) amplification is associated with poor prognosis of ovarian carcinomas across histological subtypes. Inhibitors targeting PLK1 or WEE1 are emerging as promising therapeutic agents for cancer treatment that disrupt the critical G2/M checkpoint, leading to cancer cell death. However, biomarkers that predict the response to these inhibitors are not well defined. Here, we evaluated the efficacy of the PLK1 inhibitor, volasertib, and the WEE1 inhibitor, adavosertib, along with the biomarker potential of cyclin E1 in ovarian cancer cells. Both inhibitors suppressed the proliferation of cyclin E1-overexpressing cells to a greater extent than that of cells exhibiting low cyclin E1 expression. TP53 silencing did not increase the sensitivity to these inhibitors. In cyclin E1-overexpressing cells, PLK1 inhibition reduced the proportion of cells in the G1 phase and increased those in the G2/M and sub-G1 phases. WEE1 inhibition reduced G1 phase cells without a clear peak in the S-G2/M phase and increased the sub-G1 phase cells. Both inhibitors suppressed the growth of cyclin E1-overexpressing tumors in vivo. Taken together, cyclin E1 overexpression, regardless of TP53 status, may serve as a predictive biomarker for the efficacy of these inhibitors, offering potential personalized treatment strategies for ovarian cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.