ArticleProceedings of the National Academy of Sciences of the United States of America2006
Mechanism of Akt1 inhibition of breast cancer cell invasion reveals a protumorigenic role for TSC2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
107 citing papers in PubMed, 202 citations in OpenAlex.
- Molecular subtyping and genomic profiling expand precision medicine in refractory metastatic triple-negative breast cancer: the FUTURE trial.Cell research · 2021Trial
- Phosphorylation of plectin by Akt3 promotes triple-negative breast cancer cell invasive migration.iScience · 2025Article
- ShcD adaptor protein drives invasion of triple negative breast cancer cells by aberrant activation of EGFR signaling.Molecular oncology · 2025Article
- CDO1 phosphorylation is required for IL-6-induced tumor cell proliferation through governing cysteine availability.Cell communication and signaling : CCS · 2025Article
- Antisense RNAs (asRNAs) as key players in gallbladder cancer progression: a bioinformatics analysis.Gastroenterology and hepatology from bed to bench · 2025Article
- Protein Tyrosine Phosphatase 1B (PTP1B): A Comprehensive Review of Its Role in Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- Role of Akt/Protein Kinase B in Cancer Metastasis.Biomedicines · 2023Review
- Clinical and Genomic Characteristics of Patients with Hormone Receptor-Positive, Human Epidermal Growth Factor Receptor 2-Negative Metastatic Breast Cancer Following Progression on Cyclin-Dependent Kinase 4 and 6 Inhibitors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Article
- AKT1 mediates multiple phosphorylation events that functionally promote HSF1 activation.The FEBS journal · 2022Article
- Akt Isoforms: A Family Affair in Breast Cancer.Cancers · 2021Review
- Sevoflurane Modulates AKT Isoforms in Triple Negative Breast Cancer Cells. An Experimental Study.Current issues in molecular biology · 2021Article
- AKT3 is a key regulator of head and neck squamous cell carcinoma.Cancer science · 2021Article
- AKT1 E17K Inhibits Cancer Cell Migration by Abrogating β-Catenin Signaling.Molecular cancer research : MCR · 2021Article
- Combined inhibition of ACK1 and AKT shows potential toward targeted therapy against KRAS-mutant non-small-cell lung cancer.Bosnian journal of basic medical sciences · 2021Article
- Methyl-Donors Can Induce Apoptosis and Attenuate Both the Akt and the Erk1/2 Mediated Proliferation Pathways in Breast and Lung Cancer Cell Lines.International journal of molecular sciences · 2021Article
- Article
- The Adipokine Component in the Molecular Regulation of Cancer Cell Survival, Proliferation and Metastasis.Pathology oncology research : POR · 2021Review
- Article
- PTEN and Other PtdIns(3,4,5)PInternational journal of molecular sciences · 2020Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Akt1 is frequently up-regulated in human tumors and has been shown to accelerate cell proliferation and to suppress programmed cell death; consequently, inhibition of the activity of Akt1 has been seen as an attractive target for therapeutic intervention. Paradoxically, hyperactivation of the Akt1 oncogene can also prevent the invasive behavior that underlies progression to metastasis. Here we show that overexpression of activated myr-Akt1 in human breast cancer cells phosphorylates and thereby targets the tumor suppressor tuberous sclerosis complex 2 (TSC2) for degradation, leading to reduced Rho-GTPase activity, decreased actin stress fibers and focal adhesions, and reduced motility and invasion. Overexpression of TSC2 rescues the migration phenotype of myr-Akt1-expressing tumor cells, and high levels of TSC2 in breast cancer patients correlate with increased metastasis and reduced survival. These data indicate that the functional properties of genes designated as oncogenes or tumor suppressor genes depend on the context of the cell type and the tissues studied, and suggest the need for caution in designing therapies targeting the function of individual genes in epithelial tissues.
Indexed as
Identifiers
What OpenQuestion holds
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.