ArticleBritish journal of cancer2024
Capivasertib combines with docetaxel to enhance anti-tumour activity through inhibition of AKT-mediated survival mechanisms in prostate cancer.
Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Capivasertib Combines with Trastuzumab Deruxtecan to Enhance Antitumor Activity in HER2-Positive and HER2-Low Tumors.Molecular cancer therapeutics · 2026Article
- 20 years of taxane therapy in prostate cancer - the past, present and future.Nature reviews. Urology · 2026Review
- [Overexpression of lncRNA SNHG12 promotes docetaxel resistance of prostate cancer cells by activating PI3K/AKT signalingNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Molecular reflex testing in patients with early metastatic castration-resistant prostate cancer within the PROMPT-study.British journal of cancer · 2026Observational
- Unveiling prognostic biomarkers and immunotherapeutic insights in prostate cancer through multi-omics and machine learning.European journal of medical research · 2025Article
- Overcoming Immune Evasion in the Prostate Tumor Microenvironment: Novel Targeted Strategies to Improve Treatment Outcomes.Cancers · 2025Review
- The Precision-Guided Use of PI3K Pathway Inhibitors for the Treatment of Solid Malignancies.Biomedicines · 2025Review
- Role of multi‑omics in advancing the understanding and treatment of prostate cancer (Review).Molecular medicine reports · 2025Review
- Article
- EMC2 promotes breast cancer progression and enhances sensitivity to PDK1/AKT inhibition by deubiquitinating ENO1.International journal of biological sciences · 2025Article
- Clinical feature and gene expression analysis in low prostate-specific antigen, high-grade prostate cancer.PloS one · 2025Article
- Capivasertib: First Approved AKT inhibitor for the Treatment of Patients with Breast Cancer.Anti-cancer agents in medicinal chemistry · 2025Review
- Potent combination benefit of the AKT inhibitor capivasertib and the BCL-2 inhibitor venetoclax in diffuse large B cell lymphoma.Leukemia · 2024Article
- Important Roles of PI3K/AKT Signaling Pathway and Relevant Inhibitors in Prostate Cancer Progression.Cancer medicine · 2024Review
- Economic Evaluation of Inavolisib Combined With Palbociclib-Fulvestrant for PIK3CA-Mutated, HR+/HER2- Advanced Breast Cancer in USA.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectiveTo explore the anti-tumour activity of combining AKT inhibition and docetaxel in PTEN protein null and WT prostate tumours.
methodsMechanisms associated with docetaxel capivasertib treatment activity in prostate cancer were examined using a panel of in vivo tumour models and cell lines.
resultsCombining docetaxel and capivasertib had increased activity in PTEN null and WT prostate tumour models in vivo. In vitro short-term docetaxel treatment caused cell cycle arrest in the majority of cells. However, a sub-population of docetaxel-persister cells did not undergo G2/M arrest but upregulated phosphorylation of PI3K/AKT pathway effectors GSK3β, p70S6K, 4E-BP1, but to a lesser extent AKT. In vivo acute docetaxel treatment induced p70S6K and 4E-BP1 phosphorylation. Treating PTEN null and WT docetaxel-persister cells with capivasertib reduced PI3K/AKT pathway activation and cell cycle progression. In vitro and in vivo it reduced proliferation and increased apoptosis or DNA damage though effects were more marked in PTEN null cells. Docetaxel-persister cells were partly reliant on GSK3β as a GSK3β inhibitor AZD2858 reversed capivasertib-induced apoptosis and DNA damage.
conclusionCapivasertib can enhance anti-tumour effects of docetaxel by targeting residual docetaxel-persister cells, independent of PTEN status, to induce apoptosis and DNA damage in part through GSK3β.
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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 OpenQuestion graph.