ArticleCells2020
Targeting PI3K and AMPKα Signaling Alone or in Combination to Enhance Radiosensitivity of Triple Negative Breast Cancer.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Efficacy and Safety of Phosphatidylinositol 3-kinase Inhibitors for Patients with Breast Cancer: A Systematic Review and Meta-analysis of Randomized Controlled Trials.Current cancer drug targets · 2024Pooled it
- Tumor suppressor syntaxin binding protein 1 regulates alternative splicing of DNA repair genes related to radiation sensitivity in breast cancer cells.Oncology letters · 2026Article
- Mitochondrial protection role of oxidoreductase-like domain containing 1 in myocardial cells under hypoxia.Medical gas research · 2026Article
- Glucose metabolic reprogramming: a novel strategy to enhance radiotherapy response to triple-negative breast cancer.Frontiers in public health · 2026Review
- The Role of PI3K/AKT/mTOR Signaling in Tumor Radioresistance and Advances in Inhibitor Research.International journal of molecular sciences · 2025Review
- Inhibition of ribonucleotide reductase subunit M2 enhances the radiosensitivity of metastatic pancreatic neuroendocrine tumor.Cancer letters · 2024Article
- GluOC promotes proliferation and metastasis of TNBC through the ROCK1 signaling pathway.Cancer cell international · 2024Article
- Unveiling the Mechanisms and Therapeutic Effects of Xiaoyao Sanjie Decoction in Triple-Negative Breast Cancer: A Network Pharmacology and Experimental Validation Approach.Drug design, development and therapy · 2024Article
- The simultaneous use of CRISPR/Cas9 to knock out the PI3Kca gene with radiation to enhance radiosensitivity and inhibit tumor growth in breast cancer.Iranian journal of basic medical sciences · 2024Article
- LncRNA DUXAP8 induces breast cancer radioresistance by modulating the PI3K/AKT/mTOR pathway and the EZH2-E-cadherin/RHOB pathway.Cancer biology & therapy · 2022Article
- Computational quantification and characterization of independently evolving cellular subpopulations within tumors is critical to inhibit anti-cancer therapy resistance.Genome medicine · 2022Article
- Natural Baicalein-Rich Fraction as Radiosensitizer in Combination with Bismuth Oxide Nanoparticles and Cisplatin for Clinical Radiotherapy.International journal of nanomedicine · 2022Article
- Influence of CeInternational journal of molecular sciences · 2021Article
- TNBC: Potential Targeting of Multiple Receptors for a Therapeutic Breakthrough, Nanomedicine, and Immunotherapy.Biomedicines · 2021Review
- Akt Isoforms: A Family Affair in Breast Cancer.Cancers · 2021Review
- Article
- Role of AMPK and Akt in triple negative breast cancer lung colonization.Neoplasia (New York, N.Y.) · 2021Article
- Long Noncoding RNAs Regulate the Radioresistance of Breast Cancer.Analytical cellular pathology (Amsterdam) · 2021Review
- Modulating the Radiation Response for Improved Outcomes in Breast Cancer.JCO precision oncology · 2021Review
- Emodin Interferes With AKT1-Mediated DNA Damage and Decreases Resistance of Breast Cancer Cells to Doxorubicin.Frontiers in oncology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype and is characterized by poor survival. Radiotherapy plays an important role in treating TNBC. The purpose of this study was to determine whether inhibiting the AMP-activated protein kinase (AMPK) and phosphatidylinositol 3-kinase (PI3K) pathways alone or in combination potentiates radiotherapy in TNBC. AMPKα1 and AMPKα2 knockdown diminished cyclin D1 expression and induced G1 cell cycle arrest but did not induce apoptosis alone or in combination with radiotherapy. Next, we analyzed the role of PI3K p85α, p85β, p110α, p110β, Akt1, and Akt2 proteins on TNBC cell cycle progression and apoptosis induction. Akt1 and p110α knockdown diminished cyclin D1 expression and induced apoptosis. Silencing Akt1 promoted synergistic apoptosis induction during radiotherapy and further reduced survival after radiation. Treatment with the Akt inhibitor, MK-2206 48 h after radiotherapy decreased Akt1 levels and potentiated radiation-induced apoptosis. Together, our results demonstrate that AMPKα, p110α, and Akt1 promote TNBC proliferation and that Akt1 is a key regulator of radiosensitivity in TNBC. Importantly, combining radiotherapy with the pharmacological inhibition of Akt1 expression is a potentially promising approach for the treatment of TNBC.
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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.